The coactivator CBP stimulates human T-cell lymphotrophic virus type I Tax transactivation in vitro.

PubMed

Kashanchi, F; Duvall, J F; Kwok, R P; Lundblad, J R; Goodman, R H; Brady, J N

1998-12-18

Tax interacts with the cellular cyclic AMP-responsive element binding protein (CREB) and facilitates the binding of the coactivator CREB binding protein (CBP), forming a multimeric complex on the cyclic AMP-responsive element (CRE)-like sites in the human T-cell lymphotrophic virus type I (HTLV-I) promoter. The trimeric complex is believed to recruit additional regulatory proteins to the HTLV-I long terminal repeat, but there has been no direct evidence that CBP is required for Tax-mediated transactivation. We present evidence that Tax and CBP activate transcription from the HTLV-I 21 base pair repeats on naked DNA templates. Transcriptional activation of the HTLV-I sequences required both Tax and CBP and could be mediated by either the N-terminal activation domain of CBP or the full-length protein. Fluorescence polarization binding assays indicated that CBP does not markedly enhance the affinity of Tax for the trimeric complex. Transcription analyses suggest that CBP activates Tax-dependent transcription by promoting transcriptional initiation and reinitiation. The ability of CBP to activate the HTLV-I promoter does not involve the stabilization of Tax binding, but rather depends upon gene activation properties of the co-activator that function in the context of a naked DNA template.

The transcription elongation factor ELL2 is specifically upregulated in HTLV-1-infected T-cells and is dependent on the viral oncoprotein Tax.

PubMed

Mann, Melanie C; Strobel, Sarah; Fleckenstein, Bernhard; Kress, Andrea K

2014-09-01

The oncoprotein Tax of human T-cell leukemia virus type 1 (HTLV-1) is a potent transactivator of viral and cellular transcription. Here, we identified ELL2 as the sole transcription elongation factor to be specifically upregulated in HTLV-1-/Tax-transformed T-cells. Tax contributes to regulation of ELL2, since transient transfection of Tax increases ELL2 mRNA, Tax transactivates the ELL2 promoter, and repression of Tax results in decrease of ELL2 in transformed T-lymphocytes. However, we also measured upregulation of ELL2 in HTLV-1-transformed cells exhibiting undetectable amounts of Tax, suggesting that ELL2 can still be maintained independent of continuous Tax expression. We further show that Tax and ELL2 synergistically activate the HTLV-1 promoter, indicating that ELL2 cooperates with Tax in viral transactivation. This is supported by our findings that Tax and ELL2 accumulate in nuclear fractions and that they co-precipitate upon co-expression in transiently-transfected cells. Thus, upregulation of ELL2 could contribute to HTLV-1 gene regulation. Copyright © 2014 Elsevier Inc. All rights reserved.

PCAF interacts with tax and stimulates tax transactivation in a histone acetyltransferase-independent manner.

PubMed

Jiang, H; Lu, H; Schiltz, R L; Pise-Masison, C A; Ogryzko, V V; Nakatani, Y; Brady, J N

1999-12-01

Recent studies have shown that the p300/CREB binding protein (CBP)-associated factor (PCAF) is involved in transcriptional activation. PCAF activity has been shown strongly associated with histone acetyltransferase (HAT) activity. In this report, we present evidence for a HAT-independent transcription function that is activated in the presence of the human T-cell leukemia virus type 1 (HTLV-1) Tax protein. In vitro and in vivo GST-Tax pull-down and coimmunoprecipitation experiments demonstrate that there is a direct interaction between Tax and PCAF, independent of p300/CBP. PCAF can be recruited to the HTLV-1 Tax responsive element in the presence of Tax, and PCAF cooperates with Tax in vivo to activate transcription from the HTLV-1 LTR over 10-fold. Point mutations at Tax amino acid 318 (TaxS318A) or 319 to 320 (Tax M47), which have decreased or no activity on the HTLV-1 promoter, are defective for PCAF binding. Strikingly, the ability of PCAF to stimulate Tax transactivation is not solely dependent on the PCAF HAT domain. Two independent PCAF HAT mutants, which knock out acetyltransferase enzyme activity, activate Tax transactivation to approximately the same level as wild-type PCAF. In contrast, p300 stimulation of Tax transactivation is HAT dependent. These studies provide experimental evidence that PCAF contains a coactivator transcription function independent of the HAT activity on the viral long terminal repeat.

PCAF Interacts with Tax and Stimulates Tax Transactivation in a Histone Acetyltransferase-Independent Manner

PubMed Central

Jiang, Hua; Lu, Hanxin; Schiltz, R. Louis; Pise-Masison, Cynthia A.; Ogryzko, Vasily V.; Nakatani, Yoshihiro; Brady, John N.

1999-01-01

Recent studies have shown that the p300/CREB binding protein (CBP)-associated factor (PCAF) is involved in transcriptional activation. PCAF activity has been shown strongly associated with histone acetyltransferase (HAT) activity. In this report, we present evidence for a HAT-independent transcription function that is activated in the presence of the human T-cell leukemia virus type 1 (HTLV-1) Tax protein. In vitro and in vivo GST-Tax pull-down and coimmunoprecipitation experiments demonstrate that there is a direct interaction between Tax and PCAF, independent of p300/CBP. PCAF can be recruited to the HTLV-1 Tax responsive element in the presence of Tax, and PCAF cooperates with Tax in vivo to activate transcription from the HTLV-1 LTR over 10-fold. Point mutations at Tax amino acid 318 (TaxS318A) or 319 to 320 (Tax M47), which have decreased or no activity on the HTLV-1 promoter, are defective for PCAF binding. Strikingly, the ability of PCAF to stimulate Tax transactivation is not solely dependent on the PCAF HAT domain. Two independent PCAF HAT mutants, which knock out acetyltransferase enzyme activity, activate Tax transactivation to approximately the same level as wild-type PCAF. In contrast, p300 stimulation of Tax transactivation is HAT dependent. These studies provide experimental evidence that PCAF contains a coactivator transcription function independent of the HAT activity on the viral long terminal repeat. PMID:10567539

76 FR 22611 - Specified Tax Return Preparers Required To File Individual Income Tax Returns Using Magnetic...

Federal Register 2010, 2011, 2012, 2013, 2014

2011-04-22

... DEPARTMENT OF THE TREASURY Internal Revenue Service 26 CFR Part 301 [TD 9518] RIN 1545-BJ52 Specified Tax Return Preparers Required To File Individual Income Tax Returns Using Magnetic Media... who prepare and file individual income tax returns using magnetic media pursuant to section 6011(e)(3...

75 FR 60371 - Requirements of a Statement Disclosing Uncertain Tax Positions; Correction

Federal Register 2010, 2011, 2012, 2013, 2014

2010-09-30

... Requirements of a Statement Disclosing Uncertain Tax Positions; Correction AGENCY: Internal Revenue Service... the IRS to require corporations to file a schedule disclosing uncertain tax positions related to the tax return as required by the IRS. FOR FURTHER INFORMATION CONTACT: Kathryn Zuba, (202) 622-3400 (not...

26 CFR 55.6060-1 - Reporting requirements for tax return preparers.

Code of Federal Regulations, 2014 CFR

2014-04-01

... (CONTINUED) MISCELLANEOUS EXCISE TAXES (CONTINUED) EXCISE TAX ON REAL ESTATE INVESTMENT TRUSTS AND REGULATED INVESTMENT COMPANIES Procedure and Administration § 55.6060-1 Reporting requirements for tax return preparers...

26 CFR 55.6060-1 - Reporting requirements for tax return preparers.

Code of Federal Regulations, 2011 CFR

2011-04-01

... (CONTINUED) MISCELLANEOUS EXCISE TAXES (CONTINUED) EXCISE TAX ON REAL ESTATE INVESTMENT TRUSTS AND REGULATED INVESTMENT COMPANIES Procedure and Administration § 55.6060-1 Reporting requirements for tax return preparers...

26 CFR 55.6060-1 - Reporting requirements for tax return preparers.

Code of Federal Regulations, 2013 CFR

2013-04-01

... (CONTINUED) MISCELLANEOUS EXCISE TAXES (CONTINUED) EXCISE TAX ON REAL ESTATE INVESTMENT TRUSTS AND REGULATED INVESTMENT COMPANIES Procedure and Administration § 55.6060-1 Reporting requirements for tax return preparers...

26 CFR 55.6060-1 - Reporting requirements for tax return preparers.

Code of Federal Regulations, 2012 CFR

2012-04-01

... (CONTINUED) MISCELLANEOUS EXCISE TAXES (CONTINUED) EXCISE TAX ON REAL ESTATE INVESTMENT TRUSTS AND REGULATED INVESTMENT COMPANIES Procedure and Administration § 55.6060-1 Reporting requirements for tax return preparers...

26 CFR 55.6060-1 - Reporting requirements for tax return preparers.

Code of Federal Regulations, 2010 CFR

2010-04-01

... (CONTINUED) MISCELLANEOUS EXCISE TAXES (CONTINUED) EXCISE TAX ON REAL ESTATE INVESTMENT TRUSTS AND REGULATED INVESTMENT COMPANIES Procedure and Administration § 55.6060-1 Reporting requirements for tax return preparers...

HTLV-1 Tax-Induced Rapid Senescence Is Driven by the Transcriptional Activity of NF-κB and Depends on Chronically Activated IKKα and p65/RelA

PubMed Central

Ho, Yik-Khuan; Zhi, Huijun; DeBiaso, Dominic; Philip, Subha; Shih, Hsiu-Ming

2012-01-01

The HTLV-1 oncoprotein Tax is a potent activator of classical and alternative NF-κB pathways and is thought to promote cell proliferation and transformation via NF-κB activation. We showed recently that hyperactivation of NF-κB by Tax triggers a cellular senescence response (H. Zhi et al., PLoS Pathog. 7:e1002025, 2011). Inhibition of NF-κB activation by expression of I-κBα superrepressor or by small hairpin RNA (shRNA)-mediated knockdown of p65/RelA rescues cells from Tax-induced rapid senescence (Tax-IRS). Here we demonstrate that Tax-IRS is driven by the transcriptional activity of NF-κB. Knockdown of IKKγ, the primary Tax target, by shRNAs abrogated Tax-mediated activation of both classical and alternative NF-κB pathways and rendered knockdown cells resistant to Tax-IRS. Consistent with a critical role of IKKα in the transcriptional activity of NF-κB, IKKα deficiency drastically decreased NF-κB trans-activation by Tax, although it only modestly reduced Tax-mediated I-κBα degradation and NF-κB nuclear localization. In contrast, although IKKβ knockdown attenuated Tax-induced NF-κB transcriptional activation, the residual NF-κB activation in IKKβ-deficient cells was sufficient to trigger Tax-IRS. Importantly, the phenotypes of NIK and TAK1 knockdown were similar to those of IKKα and IKKβ knockdown, respectively. Finally, double knockdown of RelB and p100 had a minor effect on senescence induction by Tax. These data suggest that Tax, through its interaction with IKKγ, helps recruit NIK and TAK1 for IKKα and IKKβ activation, respectively. In the presence of Tax, the delineation between the classical and alternative NF-κB pathways becomes obscured. The senescence checkpoint triggered by Tax is driven by the transcriptional activity of NF-κB, which depends on activated IKKα and p65/RelA. PMID:22740410

Tax-exempt hospitals and community benefits: a review of state reporting requirements.

PubMed

Hellinger, Fred Joseph

2009-02-01

In June 2007 the Internal Revenue Service proposed a major overhaul of its reporting requirements for tax-exempt hospitals and released draft Form 990 (the IRS form filed by tax-exempt organizations each year). In December 2007 the IRS promulgated the final Form 990 after incorporating some of the recommendations made in the almost seven hundred public comments on the discussion draft. One recommendation adopted in the final Form 990 is the postponement until tax year 2009 (returns filed in 2010) of the requirement for hospitals to submit detailed information on the percentage of total expenses attributable to charity care, unreimbursed Medicaid costs, and community-health improvement programs (the discussion draft required this information for tax year 2007). Although the IRS will not require tax-exempt hospitals to provide detailed information about community benefits until the 2009 tax year, sixteen states have laws requiring tax-exempt hospitals to enumerate the benefits that they provide to the community. Information about the impact of these laws on the provision of community benefits (e.g., charity and uncompensated care) is examined in this study whose primary purpose is to highlight information policy makers may glean from states that have adopted community-benefit reporting laws.

26 CFR 1.6011-7 - Specified tax return preparers required to file individual income tax returns using magnetic media.

Code of Federal Regulations, 2014 CFR

2014-04-01

... individual income tax returns using magnetic media. 1.6011-7 Section 1.6011-7 Internal Revenue INTERNAL... tax returns using magnetic media. Individual income tax returns that are required to be filed on magnetic media by tax return preparers under section 6011(e)(3) and § 301.6011-7 of this chapter must be...

26 CFR 1.6011-7 - Specified tax return preparers required to file individual income tax returns using magnetic media.

Code of Federal Regulations, 2012 CFR

2012-04-01

... individual income tax returns using magnetic media. 1.6011-7 Section 1.6011-7 Internal Revenue INTERNAL... tax returns using magnetic media. Individual income tax returns that are required to be filed on magnetic media by tax return preparers under section 6011(e)(3) and § 301.6011-7 of this chapter must be...

26 CFR 1.6011-7 - Specified tax return preparers required to file individual income tax returns using magnetic media.

Code of Federal Regulations, 2011 CFR

2011-04-01

... individual income tax returns using magnetic media. 1.6011-7 Section 1.6011-7 Internal Revenue INTERNAL... tax returns using magnetic media. Individual income tax returns that are required to be filed on magnetic media by tax return preparers under section 6011(e)(3) and § 301.6011-7 of this chapter must be...

75 FR 76940 - Specified Tax Return Preparers Required To File Individual Income Tax Returns Using Magnetic...

Federal Register 2010, 2011, 2012, 2013, 2014

2010-12-10

... DEPARTMENT OF THE TREASURY Internal Revenue Service 26 CFR Parts 1 and 301 [REG-100194-10] RIN 1545-BJ52 Specified Tax Return Preparers Required To File Individual Income Tax Returns Using Magnetic Media; Correction AGENCY: Internal Revenue Service (IRS), Treasury. ACTION: Correction to notice of...

26 CFR 157.6060-1 - Reporting requirements for tax return preparers.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 17 2010-04-01 2010-04-01 false Reporting requirements for tax return preparers. 157.6060-1 Section 157.6060-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY (CONTINUED) MISCELLANEOUS EXCISE TAXES (CONTINUED) EXCISE TAX ON STRUCTURED SETTLEMENT FACTORING TRANSACTIONS...

The HTLV-I tax protein transcriptionally modulates OX40 antigen expression.

PubMed

Pankow, R; Dürkop, H; Latza, U; Krause, H; Kunzendorf, U; Pohl, T; Bulfone-Paus, S

2000-07-01

OX40 is a member of the TNF receptor family, expressed on activated T cells. It is the only costimulatory T cell molecule known to be specifically up-regulated in human T cell leukemia virus type-I (HTLV-I)-producing cells. In a T cell line, OX40 surface expression was shown to be induced by HTLV-I Tax alone. To understand molecular mechanisms of OX40 gene regulation and modulation by HTLV-I Tax, we have cloned the human OX40 gene and analyzed its 5'-flanking region. By reporter gene analysis with progressive 5' deletions from nucleotides -1259 to -64, we have defined a 157-bp DNA fragment as a minimal promoter for constitutive expression. In addition, we show that in the OX40+ cell line, Co, Tax is able to further increase OX40 surface expression. Up-regulation of OX40 promoter activity by Tax requires two upstream NF-kappaB sites, which are not active in the constitutive OX40 expression. Their deletion abrogates Tax responsiveness in reporter gene analysis. The site-directed mutagenesis of each NF-kappaB site demonstrates that cooperative NF-kappaB binding is a prerequisite for Tax-directed activity as neither site alone is sufficient for a full Tax responsiveness of the OX40 promoter. Upon Tax expression, both sites bind p65 and c-Rel. These data provide new insight into the direct regulation of OX40 by Tax and add to our understanding of the possible role of the OX40/OX40 ligand system in the proliferation of HTLV-I+ T cells.

Insight into the tumor suppressor function of CBP through the viral oncoprotein tax.

PubMed

Van Orden, K; Nyborg, J K

2000-01-01

CREB binding protein (CBP) is a cellular coactivator protein that regulates essentially all known pathways of gene expression. The transcriptional coactivator properties of CBP are utilized by at least 25 different transcription factors representing nearly all known classes of DNA binding proteins. Once bound to their target genes, these transcription factors are believed to tether CBP to the promoter, leading to activated transcription. CBP functions to stimulate transcription through direct recruitment of the general transcription machinery as well as acetylation of both histone and transcription factor substrates. Recent observations indicate that a critical dosage of CBP is required for normal development and tumor suppression, and that perturbations in CBP concentrations may disrupt cellular homeostasis. Furthermore, there is accumulating evidence that CBP deregulation plays a direct role in hematopoietic malignancies. However, the molecular events linking CBP deregulation and malignant transformation are unclear. Further insight into the function of CBP, and its role as a tumor suppressor, can be gained through recent studies of the human T-cell leukemia virus, type I (HTLV-I) Tax oncoprotein. Tax is known to utilize CBP to stimulate transcription from the viral promoter. However, recent data suggest that as a consequence of the Tax-CBP interaction, many cellular transcription factor pathways may be deregulated. Tax disruption of CBP function may play a key role in transformation of the HTLV-I-infected cell. Thus, Tax derailment of CBP may lend important information about the tumor suppressor properties of CBP and serve as a model for the role of CBP in hematopoietic malignancies.

Tax Abolishes Histone H1 Repression of p300 Acetyltransferase Activity at the Human T-Cell Leukemia Virus Type 1 Promoter▿

PubMed Central

Konesky, Kasey L.; Nyborg, Jennifer K.; Laybourn, Paul J.

2006-01-01

Upon infection of human T-cell leukemia virus type 1 (HTLV-1), the provirus is integrated into the host cell genome and subsequently packaged into chromatin that contains histone H1. Consequently, transcriptional activation of the virus requires overcoming the environment of chromatin and H1. To efficiently activate transcription, HTLV-1 requires the virally encoded protein Tax and cellular transcription factor CREB. Together Tax and CREB interact with three cis-acting promoter elements called viral cyclic-AMP response elements (vCREs). Binding of Tax and CREB to the vCREs promotes association of p300/CBP into the complex and leads to transcriptional activation. Therefore, to fully understand the mechanism of Tax transactivation, it is necessary to examine transcriptional activation from chromatin assembled with H1. Using a DNA template harboring the complete HTLV-1 promoter sequence and a highly defined recombinant assembly system, we demonstrate proper incorporation of histone H1 into chromatin. Addition of H1 to the chromatin template reduces HTLV-1 transcriptional activation through a novel mechanism. Specifically, H1 does not inhibit CREB or Tax binding to the vCREs or p300 recruitment to the promoter. Rather, H1 directly targets p300 acetyltransferase activity. Interestingly, in determining the mechanism of H1 repression, we have discovered a previously undefined function of Tax, overcoming the repressive effects of H1-chromatin. Tax specifically abrogates the H1 repression of p300 enzymatic activity in a manner independent of p300 recruitment and without displacement of H1 from the promoter. PMID:16943293

Interaction of HTLV-1 Tax protein with calreticulin: implications for Tax nuclear export and secretion.

PubMed

Alefantis, Timothy; Flaig, Katherine E; Wigdahl, Brian; Jain, Pooja

2007-05-01

Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent of adult T cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 transcriptional transactivator protein Tax plays an integral role in virus replication and disease progression. Traditionally, Tax is described as a nuclear protein where it performs its primary role as a transcriptional transactivator. However, recent studies have clearly shown that Tax can also be localized to the cytoplasm where it has been shown to interact with a number of host transcription factors most notably NF-kappaB, constitutive expression of which is directly related to the T cell transforming properties of Tax in ATL patients. The presence of a functional nuclear export signal (NES) within Tax and the secretion of full-length Tax have also been demonstrated previously. Additionally, release of Tax from HTLV-1-infected cells and the presence of cell-free Tax was demonstrated in the CSF of HAM/TSP patients suggesting that the progression to HAM/TSP might be mediated by the ability of Tax to function as an extracellular cytokine. Therefore, in both ATL and HAM/TSP Tax nuclear export and nucleocytoplasmic shuttling may play a critical role, the mechanism of which remains unknown. In this study, we have demonstrated that the calcium binding protein calreticulin interacts with Tax by co-immunoprecipitation. This interaction was found to localize to a region at or near the nuclear membrane. In addition, differential expression of calreticulin was demonstrated in various cell types that correlated with their ability to retain cytoplasmic Tax, particularly in astrocytes. Finally, a comparison of a number of HTLV-1-infected T cell lines to non-infected T cells revealed higher expression of calreticulin in infected cells implicating a direct role for this protein in HTLV-1 infection.

An alternate property tax program requiring a forest management plan and scheduled harvesting

Treesearch

D.F. Dennis; P.E. Sendak

1991-01-01

Vermont's Use Value Appraisal property tax program, designed to address problems such as tax inequity and forced development caused by taxing agricultural and forest land based on speculative values, requires a forest management plan and scheduled harvests. A probit analysis of enrollment provides evidence of the program's success in attracting large parcels...

Activation of IKKalpha and IKKbeta through their fusion with HTLV-I tax protein.

PubMed

Xiao, G; Sun, S C

2000-10-26

Human T-cell leukemia virus type I (HTLV-I) Tax protein persistently stimulates the activity of IkappaB kinase (IKK), resulting in constitutive activation of the transcription factor NF-kappaB. Tax activation of IKK requires physical interaction of this viral protein with the IKK regulatory subunit, IKKgamma. The Tax/IKKgamma interaction allows Tax to engage the IKK catalytic subunits, IKKalpha and IKKbeta, although it remains unclear whether this linker function of IKKgamma is sufficient for supporting the Tax-specific IKK activation. To address this question, we have examined the sequences of IKKgamma required for modulating the Tax/IKK signaling. We demonstrate that when fused to Tax, a small N-terminal fragment of IKKgamma, containing its minimal IKKalpha/beta-binding domain, is sufficient for bringing Tax to and activating the IKK catalytic subunits. Disruption of the IKKalpha/beta-binding activity of this domain abolishes its function in modulating the Tax/IKK signaling. We further demonstrate that direct fusion of Tax to IKKalpha and IKKbeta leads to activation of these kinases. These findings suggest that the IKKgamma-directed Tax/IKK association serves as a molecular trigger for IKK activation.

26 CFR 301.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2012 CFR

2012-04-01

... 26 Internal Revenue 18 2012-04-01 2012-04-01 false Required use of magnetic media for corporate... Returns Returns and Records § 301.6011-5 Required use of magnetic media for corporate income tax returns. (a) Corporate income tax returns required on magnetic media—(1) A corporation required to file a...

26 CFR 301.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2013 CFR

2013-04-01

... 26 Internal Revenue 18 2013-04-01 2013-04-01 false Required use of magnetic media for corporate... Returns Returns and Records § 301.6011-5 Required use of magnetic media for corporate income tax returns. (a) Corporate income tax returns required on magnetic media—(1) A corporation required to file a...

26 CFR 301.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2014 CFR

2014-04-01

... 26 Internal Revenue 18 2014-04-01 2014-04-01 false Required use of magnetic media for corporate... Returns Returns and Records § 301.6011-5 Required use of magnetic media for corporate income tax returns. (a) Corporate income tax returns required on magnetic media—(1) A corporation required to file a...

26 CFR 301.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 18 2011-04-01 2011-04-01 false Required use of magnetic media for corporate... Returns Returns and Records § 301.6011-5 Required use of magnetic media for corporate income tax returns. (a) Corporate income tax returns required on magnetic media—(1) A corporation required to file a...

26 CFR 301.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 18 2010-04-01 2010-04-01 false Required use of magnetic media for corporate... Returns Returns and Records § 301.6011-5 Required use of magnetic media for corporate income tax returns. (a) Corporate income tax returns required on magnetic media—(1) A corporation required to file a...

SMYD3 interacts with HTLV-1 Tax and regulates subcellular localization of Tax.

PubMed

Yamamoto, Keiyu; Ishida, Takaomi; Nakano, Kazumi; Yamagishi, Makoto; Yamochi, Tadanori; Tanaka, Yuetsu; Furukawa, Yoichi; Nakamura, Yusuke; Watanabe, Toshiki

2011-01-01

HTLV-1 Tax deregulates signal transduction pathways, transcription of genes, and cell cycle regulation of host cells, which is mainly mediated by its protein-protein interactions with host cellular factors. We previously reported an interaction of Tax with a histone methyltransferase (HMTase), SUV39H1. As the interaction was mediated by the SUV39H1 SET domain that is shared among HMTases, we examined the possibility of Tax interaction with another HMTase, SMYD3, which methylates histone H3 lysine 4 and activates transcription of genes, and studied the functional effects. Expression of endogenous SMYD3 in T cell lines and primary T cells was confirmed by immunoblotting analysis. Co-immuno-precipitaion assays and in vitro pull-down assay indicated interaction between Tax and SMYD3. The interaction was largely dependent on the C-terminal 180 amino acids of SMYD3, whereas the interacting domain of Tax was not clearly defined, although the N-terminal 108 amino acids were dispensable for the interaction. In the cotransfected cells, colocalization of Tax and SMYD3 was indicated in the cytoplasm or nuclei. Studies using mutants of Tax and SMYD3 suggested that SMYD3 dominates the subcellular localization of Tax. Reporter gene assays showed that nuclear factor-κB activation promoted by cytoplasmic Tax was enhanced by the presence of SMYD3, and attenuated by shRNA-mediated knockdown of SMYD3, suggesting an increased level of Tax localization in the cytoplasm by SMYD3. Our study revealed for the first time Tax-SMYD3 direct interaction, as well as apparent tethering of Tax by SMYD3, influencing the subcellular localization of Tax. Results suggested that SMYD3-mediated nucleocytoplasmic shuttling of Tax provides one base for the pleiotropic effects of Tax, which are mediated by the interaction of cellular proteins localized in the cytoplasm or nucleus. © 2010 Japanese Cancer Association.

The HTLV-1 Tax Oncoprotein Represses Ku80 Gene Expression

PubMed Central

Ducu, Razvan I.; Dayaram, Tajhal; Marriott, Susan J.

2011-01-01

The HTLV-I oncoprotein Tax interferes with DNA double strand break repair. Since non-homologous end joining (NHEJ) is a major pathway used to repair DNA double strand breaks we examined the effect of Tax on this pathway, with particular interest in the expression and function of Ku80, a critical component of the NHEJ pathway. Tax expression decreased Ku80 mRNA and protein levels, and repressed transcription from the Ku80 promoter. Conversely, Ku80 mRNA increased following siRNA knockdown of Tax in HTLV-I infected cells. Tax expression was associated with an elevated number of micronuclei and nucleoplasmic bridges, hallmarks of improper DNA double strand break repair. Our studies identified Tax as a transcriptional repressor of Ku80 that correlates with decreased DNA repair function. The reduction of Ku80 transcription by Tax may deplete the cell of an essential DNA break binding protein, resulting in reduced repair of DNA double strand breaks and accumulation genomic mutations. PMID:21571351

Proposed regs address new hospital tax-exemption requirements.

PubMed

Speizman, Richard A; Moore, V A; Mitchell, Alexandra O

2013-03-01

Proposed regulations set forth detailed rules for implementing the new tax-exemption requirements of Section 501(r) of the Internal Revenue Code for not-for-profit organizations operating hospital facilities. The proposed regulations provide guidance on the written financial assistance policies (FAPs) that hospital facilities are required to establish. The regulations propose methodologies for determining the amounts that a hospital facility can charge FAP-eligible individuals for emergency and other medically necessary care. They prescribe procedures that hospital facilities would be required to follow before engaging in extraordinary collection actions against an individual.

An extensive requirement for transcription factor IID-specific TAF-1 in Caenorhabditis elegans embryonic transcription.

PubMed

Walker, Amy K; Shi, Yang; Blackwell, T Keith

2004-04-09

The general transcription factor TFIID sets the mRNA start site and consists of TATA-binding protein and associated factors (TAF(II)s), some of which are also present in SPT-ADA-GCN5 (SAGA)-related complexes. In yeast, results of multiple studies indicate that TFIID-specific TAF(II)s are not required for the transcription of most genes, implying that intact TFIID may have a surprisingly specialized role in transcription. Relatively little is known about how TAF(II)s contribute to metazoan transcription in vivo, especially at developmental and tissue-specific genes. Previously, we investigated functions of four shared TFIID/SAGA TAF(II)s in Caenorhabditis elegans. Whereas TAF-4 was required for essentially all embryonic transcription, TAF-5, TAF-9, and TAF-10 were dispensable at multiple developmental and other metazoan-specific promoters. Here we show evidence that in C. elegans embryos transcription of most genes requires TFIID-specific TAF-1. TAF-1 is not as universally required as TAF-4, but it is essential for a greater proportion of transcription than TAF-5, -9, or -10 and is important for transcription of many developmental and other metazoan-specific genes. TAF-2, which binds core promoters with TAF-1, appears to be required for a similarly substantial proportion of transcription. C. elegans TAF-1 overlaps functionally with the coactivator p300/CBP (CBP-1), and at some genes it is required along with the TBP-like protein TLF(TRF2). We conclude that during C. elegans embryogenesis TAF-1 and TFIID have broad roles in transcription and development and that TFIID and TLF may act together at certain promoters. Our findings imply that in metazoans TFIID may be of widespread importance for transcription and for expression of tissue-specific genes.

26 CFR 1.6695-2 - Tax return preparer due diligence requirements for determining earned income credit eligibility.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 13 2010-04-01 2010-04-01 false Tax return preparer due diligence requirements... the Tax, Additional Amounts, and Assessable Penalties § 1.6695-2 Tax return preparer due diligence requirements for determining earned income credit eligibility. (a) Penalty for failure to meet due diligence...

A Luciferase Functional Quantitative Assay for Measuring NF-ĸB Promoter Transactivation Mediated by HTLV-1 and HTLV-2 Tax Proteins.

PubMed

Bergamo, Elisa; Diani, Erica; Bertazzoni, Umberto; Romanelli, Maria Grazia

2017-01-01

HTLV-1 and HTLV-2 viruses express Tax transactivator proteins required for viral genome transcription and capable of transforming cells in vivo and in vitro. Although Tax oncogenic potential needs to be further elucidated, it is well established that Tax proteins activate, among others, transcription factors of the NF-ĸB family, which are involved in immune and inflammatory responses, cell growth, apoptosis, stress responses and oncogenesis. Here, we describe a reporter gene assay applied for quantitative analysis of Tax-dependent NF-ĸB activation. The procedure is based on co-transfection of two individual vectors containing the cDNA for firefly and Renilla luciferase enzymes and vectors expressing Tax proteins. The luciferase expression is driven by cis-NF-ĸB promoter regulatory elements responsive to Tax transactivating factor. This assay is particularly useful to investigate Tax influence on NF-ĸB activation mediated by viral or host factors.

Hijacking of the O-GlcNAcZYME complex by the HTLV-1 Tax oncoprotein facilitates viral transcription

PubMed Central

Waast, Laetitia; Kuo, Mei-Shiue; Mangeney, Marianne; Martella, Christophe; Souidi, Mouloud; Issad, Tarik

2017-01-01

The viral Tax oncoprotein plays a key role in both Human T-cell lymphotropic virus type 1 (HTLV-1)-replication and HTLV-1-associated pathologies, notably adult T-cell leukemia. Tax governs the transcription from the viral 5’LTR, enhancing thereby its own expression, via the recruitment of dimers of phosphorylated CREB to cAMP-response elements located within the U3 region (vCRE). In addition to phosphorylation, CREB is also the target of O-GlcNAcylation, another reversible post-translational modification involved in a wide range of diseases, including cancers. O-GlcNAcylation consists in the addition of O-linked-N-acetylglucosamine (O-GlcNAc) on Serine or Threonine residues, a process controlled by two enzymes: O-GlcNAc transferase (OGT), which transfers O-GlcNAc on proteins, and O-GlcNAcase (OGA), which removes it. In this study, we investigated the status of O-GlcNAcylation enzymes in HTLV-1-transformed T cells. We found that OGA mRNA and protein expression levels are increased in HTLV-1-transformed T cells as compared to control T cell lines while OGT expression is unchanged. However, higher OGA production coincides with a reduction in OGA specific activity, showing that HTLV-1-transformed T cells produce high level of a less active form of OGA. Introducing Tax into HEK-293T cells or Tax-negative HTLV-1-transformed TL-om1 T cells is sufficient to inhibit OGA activity and increase total O-GlcNAcylation, without any change in OGT activity. Furthermore, Tax interacts with the OGT/OGA complex and inhibits the activity of OGT-bound OGA. Pharmacological inhibition of OGA increases CREB O-GlcNAcylation as well as HTLV-1-LTR transactivation by Tax and CREB recruitment to the LTR. Moreover, overexpression of wild-type CREB but not a CREB protein mutated on a previously described O-GlcNAcylation site enhances Tax-mediated LTR transactivation. Finally, both OGT and OGA are recruited to the LTR. These findings reveal the interplay between Tax and the O

Hijacking of the O-GlcNAcZYME complex by the HTLV-1 Tax oncoprotein facilitates viral transcription.

PubMed

Groussaud, Damien; Khair, Mostafa; Tollenaere, Armelle I; Waast, Laetitia; Kuo, Mei-Shiue; Mangeney, Marianne; Martella, Christophe; Fardini, Yann; Coste, Solène; Souidi, Mouloud; Benit, Laurence; Pique, Claudine; Issad, Tarik

2017-07-01

The viral Tax oncoprotein plays a key role in both Human T-cell lymphotropic virus type 1 (HTLV-1)-replication and HTLV-1-associated pathologies, notably adult T-cell leukemia. Tax governs the transcription from the viral 5'LTR, enhancing thereby its own expression, via the recruitment of dimers of phosphorylated CREB to cAMP-response elements located within the U3 region (vCRE). In addition to phosphorylation, CREB is also the target of O-GlcNAcylation, another reversible post-translational modification involved in a wide range of diseases, including cancers. O-GlcNAcylation consists in the addition of O-linked-N-acetylglucosamine (O-GlcNAc) on Serine or Threonine residues, a process controlled by two enzymes: O-GlcNAc transferase (OGT), which transfers O-GlcNAc on proteins, and O-GlcNAcase (OGA), which removes it. In this study, we investigated the status of O-GlcNAcylation enzymes in HTLV-1-transformed T cells. We found that OGA mRNA and protein expression levels are increased in HTLV-1-transformed T cells as compared to control T cell lines while OGT expression is unchanged. However, higher OGA production coincides with a reduction in OGA specific activity, showing that HTLV-1-transformed T cells produce high level of a less active form of OGA. Introducing Tax into HEK-293T cells or Tax-negative HTLV-1-transformed TL-om1 T cells is sufficient to inhibit OGA activity and increase total O-GlcNAcylation, without any change in OGT activity. Furthermore, Tax interacts with the OGT/OGA complex and inhibits the activity of OGT-bound OGA. Pharmacological inhibition of OGA increases CREB O-GlcNAcylation as well as HTLV-1-LTR transactivation by Tax and CREB recruitment to the LTR. Moreover, overexpression of wild-type CREB but not a CREB protein mutated on a previously described O-GlcNAcylation site enhances Tax-mediated LTR transactivation. Finally, both OGT and OGA are recruited to the LTR. These findings reveal the interplay between Tax and the O-GlcNAcylation pathway

Coactivator-associated arginine methyltransferase 1 enhances transcriptional activity of the human T-cell lymphotropic virus type 1 long terminal repeat through direct interaction with Tax.

PubMed

Jeong, Soo-Jin; Lu, Hanxin; Cho, Won-Kyung; Park, Hyeon Ung; Pise-Masison, Cynthia; Brady, John N

2006-10-01

In this study, we demonstrate that the coactivator-associated arginine methyltransferase 1 (CARM1), which methylates histone H3 and other proteins such as p300/CBP, is positively involved in the regulation of Tax transactivation. First, transfection studies demonstrated that overexpression of CARM1 wild-type protein resulted in increased Tax transactivation of the human T-cell lymphotropic virus type 1 (HTLV-1) long terminal repeat (LTR). In contrast, transfection of a catalytically inactive CARM1 methyltransferase mutant did not enhance Tax transactivation. CARM1 facilitated Tax transactivation of the CREB-dependent cellular GEM promoter. A direct physical interaction between HTLV-1 Tax and CARM1 was demonstrated using in vitro glutathione S-transferase-Tax binding assays, in vivo coimmunoprecipitation, and confocal microscopy experiments. Finally, chromatin immunoprecipitation analysis of the activated HTLV-1 LTR promoter showed the association of CARM1 and methylated histone H3 with the template DNA. In vitro, Tax facilitates the binding of CARM1 to the transcription complex. Together, our data provide evidence that CARM1 enhances Tax transactivation of the HTLV-1 LTR through a direct interaction between CARM1 and Tax and this binding promotes methylation of histone H3 (R2, R17, and R26).

Factor requirements for transcription in the Archaeon Sulfolobus shibatae.

PubMed

Qureshi, S A; Bell, S D; Jackson, S P

1997-05-15

Archaea (archaebacteria) constitute a domain of life that is distinct from Bacteria (eubacteria) and Eucarya (eukaryotes). Although archaeal cells share many morphological features with eubacteria, their transcriptional apparatus is more akin to eukaryotic RNA polymerases I, II and III than it is to eubacterial transcription systems. Thus, in addition to possessing a 10 subunit RNA polymerase and a homologue of the TATA-binding protein (TBP), Archaea possess a polypeptide termed TFB that is homologous to eukaryotic TFIIB. Here, we investigate the factor requirements for transcription of several promoters of the archaeon Sulfolobus shibatae and its associated virus SSV. Through in vitro transcription and immunodepletion, we demonstrate that S. shibatae TBP, TFB and RNA polymerase are not complexed tightly with one another and that each is required for efficient transcription of all promoters tested. Furthermore, full transcription is restored by supplementing respective depleted extracts with recombinant TBP or TFB, indicating that TBP-associated factors or TFB-associated factors are not required. Indeed, gel-filtration suggests that Sulfolobus TBP and TFB are not associated stably with other proteins. Finally, all promoters analysed are transcribed accurately and efficiently in an in vitro system comprising recombinant TBP and TFB, together with essentially homogeneous preparation of RNA polymerase. Transcription in Archaea is therefore fundamentally homologous to that in eukaryotes, although factor requirements appear to be much less complex.

The PDZ protein tax-interacting protein-1 inhibits beta-catenin transcriptional activity and growth of colorectal cancer cells.

PubMed

Kanamori, Mutsumi; Sandy, Peter; Marzinotto, Stefania; Benetti, Roberta; Kai, Chikatoshi; Hayashizaki, Yoshihide; Schneider, Claudio; Suzuki, Harukazu

2003-10-03

Wnt signaling is essential during development while deregulation of this pathway frequently leads to the formation of various tumors including colorectal carcinomas. A key component of the pathway is beta-catenin that, in association with TCF-4, directly regulates the expression of Wnt-responsive genes. To identify novel binding partners of beta-catenin that may control its transcriptional activity, we performed a mammalian two-hybrid screen and isolated the Tax-interacting protein (TIP-1). The in vivo complex formation between beta-catenin and TIP-1 was verified by coimmunoprecipitation, and a direct physical association was revealed by glutathione S-transferase pull-down experiments in vitro. By using a panel of deletion mutants of both proteins, we demonstrate that the interaction is mediated by the PDZ (PSD-95/DLG/ZO-1 homology) domain of TIP-1 and requires primarily the last four amino acids of beta-catenin. TIP-1 overexpression resulted in a dose-dependent decrease in the transcriptional activity of beta-catenin when tested on the TOP/FOPFLASH reporter system. Conversely, siRNA-mediated knock-down of endogenous TIP-1 slightly increased endogenous beta-catenin transactivation function. Moreover, we show that overexpression of TIP-1 reduced the proliferation and anchorage-independent growth of colorectal cancer cells. These data suggest that TIP-1 may represent a novel regulatory element in the Wnt/beta-catenin signaling pathway.

75 FR 54802 - Requirement of a Statement Disclosing Uncertain Tax Positions

Federal Register 2010, 2011, 2012, 2013, 2014

2010-09-09

... return. Corporations that prepare financial statements are required by generally accepted accounting principles to identify and quantify all uncertain tax positions as described in Financial Accounting..., including International Financial Reporting Standards and country-specific generally accepted accounting...

76 FR 36905 - Information Collection Requirement; Defense Federal Acquisition Regulation Supplement; Taxes

Federal Register 2010, 2011, 2012, 2013, 2014

2011-06-23

... DEPARTMENT OF DEFENSE Defense Acquisition Regulations System Information Collection Requirement; Defense Federal Acquisition Regulation Supplement; Taxes AGENCY: Defense Acquisition Regulations System, Department of Defense (DoD). [[Page 36906

Cloning of Novel Isoforms of the Human Gli2 Oncogene and Their Activities To Enhance Tax-Dependent Transcription of the Human T-Cell Leukemia Virus Type 1 Genome

PubMed Central

Tanimura, Akira; Dan, Shingo; Yoshida, Mitsuaki

1998-01-01

The expression of human T-cell leukemia virus type 1 (HTLV-1) is activated by interaction of a viral transactivator protein, Tax, and cellular transcription factor, CREB (cyclic AMP response element binding protein), which bind to a 21-bp enhancer in the long terminal repeats (LTR). THP (Tax-helping protein) was previously determined to enhance the transactivation by Tax protein. Here we report novel forms of the human homolog of a member of the Gli oncogene family, Gli2 (also termed Gli2/THP), an extended form of a zinc finger protein, THP, which was described previously. Four possible isoforms (hGli2 α, β, γ, and δ) are formed by combinations of two independent alternative splicings, and all the isoforms could bind to a DNA motif, TRE2S, in the LTR. The longer isoforms, α and β, were abundantly expressed in various cell lines including HTLV-1-infected T-cell lines. Fusion proteins of the hGli2 isoforms with the DNA-binding domain of Gal4 activated transcription when the reporter contained a Gal4-binding site and one copy of the 21-bp sequence, to which CREB binds. This activation was observed only in the presence of Tax. The 21-bp sequence in the reporter was also essential for the activation. These results suggest that simultaneous binding of hGli2 and CREB to the respective sites in the reporter seems to be critical for Tax protein to activate transcription. Consequently, it is probable that the LTR can be regulated by two independent signals through hGli2 and CREB, since the LTR contains the 21-bp and TRE2S sequences in the vicinity. PMID:9557682

Molecular interactions involved in the transactivation of the human T-cell leukemia virus type 1 promoter mediated by Tax and CREB-2 (ATF-4).

PubMed

Gachon, F; Thebault, S; Peleraux, A; Devaux, C; Mesnard, J M

2000-05-01

The human T-cell leukemia virus type 1 (HTLV-1) Tax protein activates viral transcription through three 21-bp repeats located in the U3 region of the HTLV-1 long terminal repeat and called Tax-responsive elements (TxREs). Each TxRE contains nucleotide sequences corresponding to imperfect cyclic AMP response elements (CRE). In this study, we demonstrate that the bZIP transcriptional factor CREB-2 is able to bind in vitro to the TxREs and that CREB-2 binding to each of the 21-bp motifs is enhanced by Tax. We also demonstrate that Tax can weakly interact with CREB-2 bound to a cellular palindromic CRE motif such as that found in the somatostatin promoter. Mutagenesis of Tax and CREB-2 demonstrates that both N- and C-terminal domains of Tax and the C-terminal region of CREB-2 are required for direct interaction between the two proteins. In addition, the Tax mutant M47, defective for HTLV-1 activation, is unable to form in vitro a ternary complex with CREB-2 and TxRE. In agreement with recent results suggesting that Tax can recruit the coactivator CREB-binding protein (CBP) on the HTLV-1 promoter, we provide evidence that Tax, CREB-2, and CBP are capable of cooperating to stimulate viral transcription. Taken together, our data highlight the major role played by CREB-2 in Tax-mediated transactivation.

Molecular Interactions Involved in the Transactivation of the Human T-Cell Leukemia Virus Type 1 Promoter Mediated by Tax and CREB-2 (ATF-4)

PubMed Central

Gachon, Frederic; Thebault, Sabine; Peleraux, Annick; Devaux, Christian; Mesnard, Jean-Michel

2000-01-01

The human T-cell leukemia virus type 1 (HTLV-1) Tax protein activates viral transcription through three 21-bp repeats located in the U3 region of the HTLV-1 long terminal repeat and called Tax-responsive elements (TxREs). Each TxRE contains nucleotide sequences corresponding to imperfect cyclic AMP response elements (CRE). In this study, we demonstrate that the bZIP transcriptional factor CREB-2 is able to bind in vitro to the TxREs and that CREB-2 binding to each of the 21-bp motifs is enhanced by Tax. We also demonstrate that Tax can weakly interact with CREB-2 bound to a cellular palindromic CRE motif such as that found in the somatostatin promoter. Mutagenesis of Tax and CREB-2 demonstrates that both N- and C-terminal domains of Tax and the C-terminal region of CREB-2 are required for direct interaction between the two proteins. In addition, the Tax mutant M47, defective for HTLV-1 activation, is unable to form in vitro a ternary complex with CREB-2 and TxRE. In agreement with recent results suggesting that Tax can recruit the coactivator CREB-binding protein (CBP) on the HTLV-1 promoter, we provide evidence that Tax, CREB-2, and CBP are capable of cooperating to stimulate viral transcription. Taken together, our data highlight the major role played by CREB-2 in Tax-mediated transactivation. PMID:10779337

Human T Cell Leukemia Virus Type 2 Tax-Mediated NF-κB Activation Involves a Mechanism Independent of Tax Conjugation to Ubiquitin and SUMO

PubMed Central

Journo, Chloé; Bonnet, Amandine; Favre-Bonvin, Arnaud; Turpin, Jocelyn; Vinera, Jennifer; Côté, Emilie; Chevalier, Sébastien Alain; Kfoury, Youmna; Bazarbachi, Ali

2013-01-01

Permanent activation of the NF-κB pathway by the human T cell leukemia virus type 1 (HTLV-1) Tax (Tax1) viral transactivator is a key event in the process of HTLV-1-induced T lymphocyte immortalization and leukemogenesis. Although encoding a Tax transactivator (Tax2) that activates the canonical NF-κB pathway, HTLV-2 does not cause leukemia. These distinct pathological outcomes might be related, at least in part, to distinct NF-κB activation mechanisms. Tax1 has been shown to be both ubiquitinated and SUMOylated, and these two modifications were originally proposed to be required for Tax1-mediated NF-κB activation. Tax1 ubiquitination allows recruitment of the IKK-γ/NEMO regulatory subunit of the IKK complex together with Tax1 into centrosome/Golgi-associated cytoplasmic structures, followed by activation of the IKK complex and RelA/p65 nuclear translocation. Herein, we compared the ubiquitination, SUMOylation, and acetylation patterns of Tax2 and Tax1. We show that, in contrast to Tax1, Tax2 conjugation to endogenous ubiquitin and SUMO is barely detectable while both proteins are acetylated. Importantly, Tax2 is neither polyubiquitinated on lysine residues nor ubiquitinated on its N-terminal residue. Consistent with these observations, Tax2 conjugation to ubiquitin and Tax2-mediated NF-κB activation is not affected by overexpression of the E2 conjugating enzyme Ubc13. We further demonstrate that a nonubiquitinable, non-SUMOylable, and nonacetylable Tax2 mutant retains a significant ability to activate transcription from a NF-κB-dependent promoter after partial activation of the IKK complex and induction of RelA/p65 nuclear translocation. Finally, we also show that Tax2 does not interact with TRAF6, a protein that was shown to positively regulate Tax1-mediated activation of the NF-κB pathway. PMID:23135727

27 CFR 70.411 - Imposition of taxes, qualification requirements, and regulations.

Code of Federal Regulations, 2014 CFR

2014-04-01

... Provisions Relating to Distilled Spirits, Wines, and Beer § 70.411 Imposition of taxes, qualification... distilled spirits (including alcohol), wine and beer. (b) Qualification requirements. Distillers, winemakers... beer which are within the jurisdiction of TTB are published in the regulations described in this...

27 CFR 70.411 - Imposition of taxes, qualification requirements, and regulations.

Code of Federal Regulations, 2013 CFR

2013-04-01

... Provisions Relating to Distilled Spirits, Wines, and Beer § 70.411 Imposition of taxes, qualification... distilled spirits (including alcohol), wine and beer. (b) Qualification requirements. Distillers, winemakers... beer which are within the jurisdiction of TTB are published in the regulations described in this...

27 CFR 70.411 - Imposition of taxes, qualification requirements, and regulations.

Code of Federal Regulations, 2011 CFR

2011-04-01

... Provisions Relating to Distilled Spirits, Wines, and Beer § 70.411 Imposition of taxes, qualification... distilled spirits (including alcohol), wine and beer. (b) Qualification requirements. Distillers, winemakers... beer which are within the jurisdiction of TTB are published in the regulations described in this...

HTLV-2B Tax oncoprotein is modified by ubiquitination and sumoylation and displays intracellular localization similar to its homologue HTLV-1 Tax

DOE Office of Scientific and Technical Information (OSTI.GOV)

Turci, Marco; Lodewick, Julie; Righi, Paola

HTLV-1 is more pathogenic than HTLV-2B. The difference is generally attributed to the properties of their individual transactivating Tax proteins. By using internal Flag-6His tagged Tax-1 and Tax-2B, which display transcriptional activities comparable to the untagged proteins and can be recognized by a single anti-Flag antibody, we demonstrate that Tax-2B is modified by ubiquitination and sumoylation. In addition, Tax2B is distributed in punctuate nuclear structures that include the RelA subunit of NF-{kappa}B, as has been previously demonstrated for Tax-1.

Tax unleashed: fulminant Tax-positive Adult T-cell Leukemia/Lymphoma after failed allogeneic stem cell transplantation.

PubMed

Ghez, David; Renand, Amédée; Lepelletier, Yves; Sibon, David; Suarez, Felipe; Rubio, Marie-Thérèse; Delarue, Richard; Buzyn, Agnès; Beljord, Kheira; Tanaka, Yuetsu; Varet, Bruno; Hermine, Olivier

2009-12-01

The human retrovirus HTLV-1 causes Adult T-cell Leukemia/Lymphoma (ATLL), a malignant lymphoproliferative disease of CD4+ T cells of dismal prognosis, in 3-5% of the 20 million infected individuals (Proietti et al.(1) and Bazarbachi et al.(2)). Infection with HTLV-1 represents a prototypical model of virus-mediated oncogenesis by virtue of the viral transactivator Tax, a potent oncogenic protein that exerts pleiotropic effects through its ability to deregulate the transcription of various cellular genes and signal transduction pathways and inhibit DNA repair enzymes, which are critical for T-cell homeostasis and genetic stability (Matsuoka and Jeang(3)) (et Boxus Retrovirology 2009). However, the oncogenic potential of Tax remains a conundrum. Tax protein expression is undetectable using conventional methods in freshly harvested ATLL cells and in non-malignant infected CD4+ T cells (Furukawa et al.(4)) but is up regulated after only a few hours of culture in vitro (Hanon et al.(5)). These observations strongly suggest that a host-derived mechanism is able to either actively repress the transcription of viral proteins in vivo or refrain the emergence of Tax-expressing cells, which would have a growth advantage. We report herein a unique case of CD4+ T-cell leukemia highly expressing Tax following rejection of an allogenic peripheral blood stem cell graft for an HTLV-1 associated lymphoma.

26 CFR 1.857-4 - Tax imposed by reason of the failure to meet certain source-of-income requirements.

Code of Federal Regulations, 2010 CFR

2010-04-01

..., DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES Real Estate Investment Trusts § 1.857-4 Tax imposed by reason of the failure to meet certain source-of-income requirements. Section 857... 26 Internal Revenue 9 2010-04-01 2010-04-01 false Tax imposed by reason of the failure to meet...

Differential transcriptional activation by human T-cell leukemia virus type 1 Tax mutants is mediated by distinct interactions with CREB binding protein and p300.

PubMed

Bex, F; Yin, M J; Burny, A; Gaynor, R B

1998-04-01

The human T-cell leukemia virus type 1 Tax protein transforms human T lymphocytes, which can lead to the development of adult T-cell leukemia. Tax transformation is related to its ability to activate gene expression via the ATF/CREB and the NF-kappaB pathways. Transcriptional activation of these pathways is mediated by the actions of the related coactivators CREB binding protein (CBP) and p300. In this study, immunocytochemistry and confocal microscopy were used to localize CBP and p300 in cells expressing wild-type Tax or Tax mutants that are able to selectively activate gene expression from either the NF-kappaB or ATF/CREB pathway. Wild-type Tax colocalized with both CBP and p300 in nuclear bodies which also contained ATF-1 and the RelA subunit of NF-kappaB. However, a Tax mutant that selectively activates gene expression from only the ATF/CREB pathway colocalized with CBP but not p300, while a Tax mutant that selectively activates gene expression from only the NF-kappaB pathway colocalized with p300 but not CBP. In vitro and in vivo protein interaction studies indicated that the integrity of two independent domains of Tax delineated by these mutants was involved in the direct interaction of Tax with either CBP or p300. These studies are consistent with a model in which activation of either the NF-kappaB or the ATF/CREB pathway by specific Tax mutants is mediated by distinct interactions with related coactivator proteins.

Distinct p300-Responsive Mechanisms Promote Caspase-Dependent Apoptosis by Human T-Cell Lymphotropic Virus Type 1 Tax Protein

PubMed Central

Nicot, Christophe; Harrod, Robert

2000-01-01

The dysregulation of cellular apoptosis pathways has emerged as a critical early event associated with the development of many types of human cancers. Numerous viral and cellular oncogenes, aside from their inherent transforming properties, are known to induce programmed cell death, consistent with the hypothesis that genetic defects are required to support tumor survival. Here, we report that nuclear expression of the CREB-binding protein (CBP)/p300-binding domain of the human T-cell lymphotropic virus type 1 (HTLV-1) transactivator, Tax, triggers an apoptotic death-inducing signal during short-term clonal analyses, as well as in transient cell death assays. Coexpression of the antiapoptotic factor Bcl-2 increased serum stimulation; incubation with the chemical caspase inhibitor z-Val-Ala-dl-Asp fluoromethylketone antagonized Tax-induced cell death. The CBP/p300-binding defective Tax mutants K88A and V89A exhibited markedly reduced cytotoxic effects compared to the wild-type Tax protein. Importantly, nuclear expression of the minimal CBP/p300-binding peptide of Tax induced apoptosis in the absence of Tax-dependent transcriptional activities, while its K88A counterpart did not cause cell death. Further, Tax-mediated apoptosis was effectively prevented by ectopic expression of the p300 coactivator. We also report that activation of the NF-κB transcription pathway by Tax, under growth arrest conditions, results in apoptosis that occurs independent of direct Tax coactivator effects. Our results allude to a novel pivotal role for the transcriptional coactivator p300 in determining cell fate and raise the possibility that dysregulated coactivator usage may pose an early barrier to transformation that must be selectively overcome as a prerequisite for the initiation of neoplasia. PMID:11046153

Distinct p300-responsive mechanisms promote caspase-dependent apoptosis by human T-cell lymphotropic virus type 1 Tax protein.

PubMed

Nicot, C; Harrod, R

2000-11-01

The dysregulation of cellular apoptosis pathways has emerged as a critical early event associated with the development of many types of human cancers. Numerous viral and cellular oncogenes, aside from their inherent transforming properties, are known to induce programmed cell death, consistent with the hypothesis that genetic defects are required to support tumor survival. Here, we report that nuclear expression of the CREB-binding protein (CBP)/p300-binding domain of the human T-cell lymphotropic virus type 1 (HTLV-1) transactivator, Tax, triggers an apoptotic death-inducing signal during short-term clonal analyses, as well as in transient cell death assays. Coexpression of the antiapoptotic factor Bcl-2 increased serum stimulation; incubation with the chemical caspase inhibitor z-Val-Ala-DL-Asp fluoromethylketone antagonized Tax-induced cell death. The CBP/p300-binding defective Tax mutants K88A and V89A exhibited markedly reduced cytotoxic effects compared to the wild-type Tax protein. Importantly, nuclear expression of the minimal CBP/p300-binding peptide of Tax induced apoptosis in the absence of Tax-dependent transcriptional activities, while its K88A counterpart did not cause cell death. Further, Tax-mediated apoptosis was effectively prevented by ectopic expression of the p300 coactivator. We also report that activation of the NF-kappaB transcription pathway by Tax, under growth arrest conditions, results in apoptosis that occurs independent of direct Tax coactivator effects. Our results allude to a novel pivotal role for the transcriptional coactivator p300 in determining cell fate and raise the possibility that dysregulated coactivator usage may pose an early barrier to transformation that must be selectively overcome as a prerequisite for the initiation of neoplasia.

A transgenic model of transactivation by the Tax protein of HTLV-I.

PubMed

Bieberich, C J; King, C M; Tinkle, B T; Jay, G

1993-09-01

The human T-lymphotropic virus type I (HTLV-I) Tax protein is a transcriptional regulatory protein that has been suggested to play a causal role in the development of several HTLV-I-associated diseases. Tax regulates expression of its own LTR and of certain cellular promoters perhaps by usurping the function of the host transcriptional machinery. We have established a transgenic mouse model system to define the spectrum of tissues in vivo that are capable of supporting Tax-mediated transcriptional transactivation. Transgenic mice carrying the HTLV-I LTR driving expression of the Escherichia coli beta-galactosidase (beta gal) gene were generated, and this LTR-beta gal gene was transcriptionally inactive in all tissues. When LTR-beta gal mice were mated to transgenic mice carrying the same LTR driving expression of the HTLV-I tax gene, mice that carried both transgenes showed restricted expression of the beta gal reporter gene in several tissues including muscle, bone, salivary glands, skin, and nerve. In addition, a dramatic increase in the number of beta gal-expressing cells was seen in response to wounding. These observations provide direct evidence for viral transactivation in vivo, delimit the tissues capable of supporting that transactivation, and provide a model system to study the mechanism of gene regulation by Tax.

SUV39H1 interacts with HTLV-1 Tax and abrogates Tax transactivation of HTLV-1 LTR

PubMed Central

Kamoi, Koju; Yamamoto, Keiyu; Misawa, Aya; Miyake, Ariko; Ishida, Takaomi; Tanaka, Yuetsu; Mochizuki, Manabu; Watanabe, Toshiki

2006-01-01

Background Tax is the oncoprotein of HTLV-1 which deregulates signal transduction pathways, transcription of genes and cell cycle regulation of host cells. Transacting function of Tax is mainly mediated by its protein-protein interactions with host cellular factors. As to Tax-mediated regulation of gene expression of HTLV-1 and cellular genes, Tax was shown to regulate histone acetylation through its physical interaction with histone acetylases and deacetylases. However, functional interaction of Tax with histone methyltransferases (HMTase) has not been studied. Here we examined the ability of Tax to interact with a histone methyltransferase SUV39H1 that methylates histone H3 lysine 9 (H3K9) and represses transcription of genes, and studied the functional effects of the interaction on HTLV-1 gene expression. Results Tax was shown to interact with SUV39H1 in vitro, and the interaction is largely dependent on the C-terminal half of SUV39H1 containing the SET domain. Tax does not affect the methyltransferase activity of SUV39H1 but tethers SUV39H1 to a Tax containing complex in the nuclei. In reporter gene assays, co-expression of SUV39H1 represses Tax transactivation of HTLV-1 LTR promoter activity, which was dependent on the methyltransferase activity of SUV39H1. Furthermore, SUV39H1 expression is induced along with Tax in JPX9 cells. Chromatin immunoprecipitation (ChIP) analysis shows localization of SUV39H1 on the LTR after Tax induction, but not in the absence of Tax induction, in JPX9 transformants retaining HTLV-1-Luc plasmid. Immunoblotting shows higher levels of SUV39H1 expression in HTLV-1 transformed and latently infected cell lines. Conclusion Our study revealed for the first time the interaction between Tax and SUV39H1 and apparent tethering of SUV39H1 by Tax to the HTLV-1 LTR. It is speculated that Tax-mediated tethering of SUV39H1 to the LTR and induction of the repressive histone modification on the chromatin through H3 K9 methylation may be the basis

Modulation of the Brd4/P-TEFb interaction by the human T-lymphotropic virus type 1 tax protein.

PubMed

Cho, Won-Kyung; Zhou, Meisheng; Jang, Moon Kyoo; Huang, Keven; Jeong, Soo-Jin; Ozato, Keiko; Brady, John N

2007-10-01

Positive transcription elongation factor (P-TEFb), which is composed of CDK9 and cyclin T1, plays an important role in cellular and viral gene expression. Our lab has recently demonstrated that P-TEFb is required for Tax transactivation of the viral long terminal repeat (LTR). P-TEFb is found in two major complexes: the inactive form, which is associated with inhibitory subunits 7SK snRNA and HEXIM1, and the active form, which is associated with, at least in part, Brd4. In this study, we analyzed the effect of Brd4 on human T-lymphotropic virus type 1 (HTLV-1) transcription. Overexpression of Brd4 repressed Tax transactivation of the HTLV-1 LTR in a dose-dependent manner. In vitro binding studies suggest that Tax and Brd4 compete for binding to P-TEFb through direct interaction with cyclin T1. Tax interacts with cyclin T1 amino acids 426 to 533, which overlaps the region responsible for Brd4 binding. In vivo, overexpression of Tax decreased the amount of 7SK snRNA associated with P-TEFb and stimulates serine 2 phosphorylation of the RNA polymerase II carboxyl-terminal domain, suggesting that Tax regulates the functionality of P-TEFb. Our results suggest the possibility that Tax may compete and functionally substitute for Brd4 in P-TEFb regulation.

Human Mitochondrial Transcription Factor B2 Is Required for Promoter Melting during Initiation of Transcription.

PubMed

Posse, Viktor; Gustafsson, Claes M

2017-02-17

The mitochondrial transcription initiation machinery in humans consists of three proteins: the RNA polymerase (POLRMT) and two accessory factors, transcription factors A and B2 (TFAM and TFB2M, respectively). This machinery is required for the expression of mitochondrial DNA and the biogenesis of the oxidative phosphorylation system. Previous experiments suggested that TFB2M is required for promoter melting, but conclusive experimental proof for this effect has not been presented. Moreover, the role of TFB2M in promoter unwinding has not been discriminated from that of TFAM. Here we used potassium permanganate footprinting, DNase I footprinting, and in vitro transcription from the mitochondrial light-strand promoter to study the role of TFB2M in transcription initiation. We demonstrate that a complex composed of TFAM and POLRMT was readily formed at the promoter but alone was insufficient for promoter melting, which only occurred when TFB2M joined the complex. We also show that mismatch bubble templates could circumvent the requirement of TFB2M, but TFAM was still required for efficient initiation. Our findings support a model in which TFAM first recruits POLRMT to the promoter, followed by TFB2M binding and induction of promoter melting. © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.

Characterization of a nuclear export signal within the human T cell leukemia virus type I transactivator protein Tax.

PubMed

Alefantis, Timothy; Barmak, Kate; Harhaj, Edward W; Grant, Christian; Wigdahl, Brian

2003-06-13

Human T cell leukemia virus type I (HTLV-I) is the etiologic agent of adult T cell leukemia and HTLV-I-associated myelopathy/tropical spastic paraparesis. The HTLV-I transactivator protein Tax plays an integral role in the etiology of adult T cell leukemia, as expression of Tax in T lymphocytes has been shown to result in immortalization. In addition, Tax is known to interface with numerous transcription factor families, including activating transcription factor/cAMP response element-binding protein and nuclear factor-kappaB, requiring Tax to localize to both the nucleus and cytoplasm. In this report, the nucleocytoplasmic localization of Tax was examined in Jurkat, HeLa, and U-87 MG cells. The results reported herein indicate that Tax contains a leucine-rich nuclear export signal (NES) that, when fused to green fluorescent protein (GFP), can direct nuclear export via the CRM-1 pathway, as determined by leptomycin B inhibition of nuclear export. However, cytoplasmic localization of full-length Tax was not altered by treatment with leptomycin B, suggesting that native Tax utilizes another nuclear export pathway. Additional support for the presence of a functional NES has also been shown because the NES mutant Tax(L200A)-GFP localized to the nuclear membrane in the majority of U-87 MG cells. Evidence has also been provided suggesting that the Tax NES likely exists as a conditionally masked signal because the truncation mutant TaxDelta214-GFP localized constitutively to the cytoplasm. These results suggest that Tax localization may be directed by specific changes in Tax conformation or by specific interactions with cellular proteins leading to changes in the availability of the Tax NES and nuclear localization signal.

Low nuclear body formation and tax SUMOylation do not prevent NF-kappaB promoter activation.

PubMed

Bonnet, Amandine; Randrianarison-Huetz, Voahangy; Nzounza, Patrycja; Nedelec, Martine; Chazal, Maxime; Waast, Laetitia; Pene, Sabrina; Bazarbachi, Ali; Mahieux, Renaud; Bénit, Laurence; Pique, Claudine

2012-09-25

The Tax protein encoded by Human T-lymphotropic virus type 1 (HTLV-1) is a powerful activator of the NF-κB pathway, a property critical for HTLV-1-induced immortalization of CD4⁺ T lymphocytes. Tax permanently stimulates this pathway at a cytoplasmic level by activating the IκB kinase (IKK) complex and at a nuclear level by enhancing the binding of the NF-κB factor RelA to its cognate promoters and by forming nuclear bodies, believed to represent transcriptionally active structures. In previous studies, we reported that Tax ubiquitination and SUMOylation play a critical role in Tax localization and NF-κB activation. Indeed, analysis of lysine Tax mutants fused or not to ubiquitin or SUMO led us to propose a two-step model in which Tax ubiquitination first intervenes to activate IKK while Tax SUMOylation is subsequently required for promoter activation within Tax nuclear bodies. However, recent studies showing that ubiquitin or SUMO can modulate Tax activities in either the nucleus or the cytoplasm and that SUMOylated Tax can serve as substrate for ubiquitination suggested that Tax ubiquitination and SUMOylation may mediate redundant rather than successive functions. In this study, we analyzed the properties of a new Tax mutant that is properly ubiquitinated, but defective for both nuclear body formation and SUMOylation. We report that reducing Tax SUMOylation and nuclear body formation do not alter the ability of Tax to activate IKK, induce RelA nuclear translocation, and trigger gene expression from a NF-κB promoter. Importantly, potent NF-κB promoter activation by Tax despite low SUMOylation and nuclear body formation is also observed in T cells, including CD4⁺ primary T lymphocytes. Moreover, we show that Tax nuclear bodies are hardly observed in HTLV-1-infected T cells. Finally, we provide direct evidence that the degree of NF-κB activation by Tax correlates with the level of Tax ubiquitination, but not SUMOylation. These data reveal that the

Low nuclear body formation and tax SUMOylation do not prevent NF-kappaB promoter activation

PubMed Central

2012-01-01

Background The Tax protein encoded by Human T-lymphotropic virus type 1 (HTLV-1) is a powerful activator of the NF-κB pathway, a property critical for HTLV-1-induced immortalization of CD4+ T lymphocytes. Tax permanently stimulates this pathway at a cytoplasmic level by activating the IκB kinase (IKK) complex and at a nuclear level by enhancing the binding of the NF-κB factor RelA to its cognate promoters and by forming nuclear bodies, believed to represent transcriptionally active structures. In previous studies, we reported that Tax ubiquitination and SUMOylation play a critical role in Tax localization and NF-κB activation. Indeed, analysis of lysine Tax mutants fused or not to ubiquitin or SUMO led us to propose a two-step model in which Tax ubiquitination first intervenes to activate IKK while Tax SUMOylation is subsequently required for promoter activation within Tax nuclear bodies. However, recent studies showing that ubiquitin or SUMO can modulate Tax activities in either the nucleus or the cytoplasm and that SUMOylated Tax can serve as substrate for ubiquitination suggested that Tax ubiquitination and SUMOylation may mediate redundant rather than successive functions. Results In this study, we analyzed the properties of a new Tax mutant that is properly ubiquitinated, but defective for both nuclear body formation and SUMOylation. We report that reducing Tax SUMOylation and nuclear body formation do not alter the ability of Tax to activate IKK, induce RelA nuclear translocation, and trigger gene expression from a NF-κB promoter. Importantly, potent NF-κB promoter activation by Tax despite low SUMOylation and nuclear body formation is also observed in T cells, including CD4+ primary T lymphocytes. Moreover, we show that Tax nuclear bodies are hardly observed in HTLV-1-infected T cells. Finally, we provide direct evidence that the degree of NF-κB activation by Tax correlates with the level of Tax ubiquitination, but not SUMOylation. Conclusions These

Beyond Transcription Factors: The Role of Chromatin Modifying Enzymes in Regulating Transcription Required for Memory

ERIC Educational Resources Information Center

Barrett, Ruth M.; Wood, Marcelo A.

2008-01-01

One of the alluring aspects of examining chromatin modifications in the role of modulating transcription required for long-term memory processes is that these modifications may provide transient and potentially stable epigenetic marks in the service of activating and/or maintaining transcriptional processes. These, in turn, may ultimately…

MOLECULAR CHARACTERIZATION OF HTLV-1 TAX INTERACTION WITH THE KIX DOMAIN OF CBP/p300

PubMed Central

Ramírez, Julita A.; Nyborg, Jennifer K.

2007-01-01

Summary The viral oncoprotein Tax mediates transcriptional activation of human T-cell leukemia virus type 1 (HTLV-1). Both Tax and the cellular transcription factor CREB bind to viral cyclic AMP response elements (vCREs) located in the viral promoter. Tax and serine 133 phosphorylated CREB (pCREB) bound to the HTLV-1 promoter facilitate viral transcription via the recruitment of the large cellular coactivators CBP/p300. While the interaction between the phosphorylated kinase inducible domain (pKID) of pCREB and the KIX domain of CBP/p300 has been well-characterized, the molecular interactions between KIX, full-length Tax, and pCREB have not been examined. In this study we biochemically characterized the interaction between Tax and KIX in a physiologically relevant complex containing pCREB and vCRE DNA. Our data show that Tax and pCREB simultaneously and independently bind two distinct surfaces on the KIX domain: Tax binds KIX at the previously-characterized mixed-lineage leukemia (MLL) protein interaction surface while pCREB binds KIX at the pKID-KIX interface. These results provide evidence for a model in which Tax and pCREB bind distinct surfaces of KIX for effective CBP/p300 recruitment to the HTLV-1 promoter. We also show that MLL competes with Tax for KIX binding, suggesting a novel mechanism of Tax oncogenesis in which normal MLL function is disrupted by Tax. PMID:17707401

Involvement of HTLV-I Tax and CREB in aneuploidy: a bioinformatics approach.

PubMed

de la Fuente, Cynthia; Gupta, Madhur V; Klase, Zachary; Strouss, Katharine; Cahan, Patrick; McCaffery, Timothy; Galante, Anthony; Soteropoulos, Patricia; Pumfery, Anne; Fujii, Masahiro; Kashanchi, Fatah

2006-07-05

Adult T-cell leukemia (ATL) is a complex and multifaceted disease associated with human T-cell leukemia virus type 1 (HTLV-I) infection. Tax, the viral oncoprotein, is considered a major contributor to cell cycle deregulation in HTLV-I transformed cells by either directly disrupting cellular factors (protein-protein interactions) or altering their transcription profile. Tax transactivates these cellular promoters by interacting with transcription factors such as CREB/ATF, NF-kappaB, and SRF. Therefore by examining which factors upregulate a particular set of promoters we may begin to understand how Tax orchestrates leukemia development. We observed that CTLL cells stably expressing wild-type Tax (CTLL/WT) exhibited aneuploidy as compared to a Tax clone deficient for CREB transactivation (CTLL/703). To better understand the contribution of Tax transactivation through the CREB/ATF pathway to the aneuploid phenotype, we performed microarray analysis comparing CTLL/WT to CTLL/703 cells. Promoter analysis of altered genes revealed that a subset of these genes contain CREB/ATF consensus sequences. While these genes had diverse functions, smaller subsets of genes were found to be involved in G2/M phase regulation, in particular kinetochore assembly. Furthermore, we confirmed the presence of CREB, Tax and RNA Polymerase II at the p97Vcp and Sgt1 promoters in vivo through chromatin immunoprecipitation in CTLL/WT cells. These results indicate that the development of aneuploidy in Tax-expressing cells may occur in response to an alteration in the transcription profile, in addition to direct protein interactions.

Distinct requirements for C.elegans TAF(II)s in early embryonic transcription.

PubMed

Walker, A K; Rothman, J H; Shi, Y; Blackwell, T K

2001-09-17

TAF(II)s are conserved components of the TFIID, TFTC and SAGA-related mRNA transcription complexes. In yeast (y), yTAF(II)17 is required broadly for transcription, but various other TAF(II)s appear to have more specialized functions. It is important to determine how TAF(II)s contribute to transcription in metazoans, which have larger and more diverse genomes. We have examined TAF(II) functions in early Caenorhabditis elegans embryos, which can survive without transcription for several cell generations. We show that taf-10 (yTAF(II)17) and taf-11 (yTAF(II)25) are required for a significant fraction of transcription, but apparently are not needed for expression of multiple developmental and other metazoan-specific genes. In contrast, taf-5 (yTAF(II)48; human TAF(II)130) seems to be required for essentially all early embryonic mRNA transcription. We conclude that TAF-10 and TAF-11 have modular functions in metazoans, and can be bypassed at many metazoan-specific genes. The broad involvement of TAF-5 in mRNA transcription in vivo suggests a requirement for either TFIID or a TFTC-like complex.

26 CFR 1.6037-2 - Required use of magnetic media for income tax returns of electing small business corporations.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 13 2010-04-01 2010-04-01 false Required use of magnetic media for income tax... Returns § 1.6037-2 Required use of magnetic media for income tax returns of electing small business... media under § 301.6037-2 of this chapter must be filed in accordance with Internal Revenue Service...

26 CFR 1.6037-2 - Required use of magnetic media for income tax returns of electing small business corporations.

Code of Federal Regulations, 2014 CFR

2014-04-01

... 26 Internal Revenue 13 2014-04-01 2014-04-01 false Required use of magnetic media for income tax...) Information Returns § 1.6037-2 Required use of magnetic media for income tax returns of electing small... magnetic media under § 301.6037-2 of this chapter must be filed in accordance with Internal Revenue Service...

26 CFR 1.6037-2 - Required use of magnetic media for income tax returns of electing small business corporations.

Code of Federal Regulations, 2012 CFR

2012-04-01

... 26 Internal Revenue 13 2012-04-01 2012-04-01 false Required use of magnetic media for income tax...) Information Returns § 1.6037-2 Required use of magnetic media for income tax returns of electing small... magnetic media under § 301.6037-2 of this chapter must be filed in accordance with Internal Revenue Service...

26 CFR 1.6037-2 - Required use of magnetic media for income tax returns of electing small business corporations.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 13 2011-04-01 2011-04-01 false Required use of magnetic media for income tax...) Information Returns § 1.6037-2 Required use of magnetic media for income tax returns of electing small... magnetic media under § 301.6037-2 of this chapter must be filed in accordance with Internal Revenue Service...

26 CFR 301.6011-7 - Specified tax return preparers required to file individual income tax returns using magnetic media.

Code of Federal Regulations, 2014 CFR

2014-04-01

...-electronic (paper) form. Submission of an individual income tax return by a tax return preparer or a... otherwise delivering of the paper individual income tax return to the IRS by the preparer, any member...) that states the taxpayer chooses to file the individual income tax return in paper format, and that the...

The Human T-Cell Leukemia Virus Type 1 Oncoprotein Tax Controls Forkhead Box O4 Activity through Degradation by the Proteasome▿

PubMed Central

Oteiza, Alexandra; Mechti, Nadir

2011-01-01

Activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway by the viral Tax oncoprotein plays a pivotal role in clonal expansion of human T-cell leukemia virus type 1 (HTLV-1)-infected cells. As the Forkhead box O (FoxO) tumor suppressors act as downstream effectors of PI3K/Akt, they represent good candidate targets whose dysregulation by Tax might be involved in HTLV-1-mediated activation and transformation of infected cells. In this report, we provide evidence showing that Tax induces a dose-dependent degradation of FoxO4 by the ubiquitin-proteasome pathway. Consistent with that, we demonstrate that Tax expression increases the interaction between FoxO4 and Mdm2 E3 ligase, leading to a strong FoxO4 polyubiquitination. These processes require the phosphorylation of FoxO4 by Akt, since a mutant of FoxO4 with mutations on its three Akt phosphorylation sites appears to be resistant to Tax-mediated degradation and ubiquitination. In addition, we show that Tax expression is associated with degradation and phosphorylation of endogenous FoxO4 in Jurkat T cells. Finally, we demonstrate that Tax represses FoxO4 transcriptional activity. Our study demonstrates that Tax can control FoxO4 protein stability and transcriptional activity and provides new insight into the subversion of cell signaling pathways during HTLV-1 infection. PMID:21525355

The RNA Export Factor, Nxt1, Is Required for Tissue Specific Transcriptional Regulation

PubMed Central

Jiang, Jianqiao; White-Cooper, Helen

2013-01-01

The highly conserved, Nxf/Nxt (TAP/p15) RNA nuclear export pathway is important for export of most mRNAs from the nucleus, by interacting with mRNAs and promoting their passage through nuclear pores. Nxt1 is essential for viability; using a partial loss of function allele, we reveal a role for this gene in tissue specific transcription. We show that many Drosophila melanogaster testis-specific mRNAs require Nxt1 for their accumulation. The transcripts that require Nxt1 also depend on a testis-specific transcription complex, tMAC. We show that loss of Nxt1 leads to reduced transcription of tMAC targets. A reporter transcript from a tMAC-dependent promoter is under-expressed in Nxt1 mutants, however the same transcript accumulates in mutants if driven by a tMAC-independent promoter. Thus, in Drosophila primary spermatocytes, the transcription factor used to activate expression of a transcript, rather than the RNA sequence itself or the core transcription machinery, determines whether this expression requires Nxt1. We additionally find that transcripts from intron-less genes are more sensitive to loss of Nxt1 function than those from intron-containing genes and propose a mechanism in which transcript processing feeds back to increase activity of a tissue specific transcription complex. PMID:23754955

50 CFR 221.56 - What are the requirements for transcription of the hearing?

Code of Federal Regulations, 2010 CFR

2010-10-01

... 50 Wildlife and Fisheries 7 2010-10-01 2010-10-01 false What are the requirements for transcription of the hearing? 221.56 Section 221.56 Wildlife and Fisheries NATIONAL MARINE FISHERIES SERVICE... requirements for transcription of the hearing? (a) Transcript and reporter's fees. The hearing will be...

50 CFR 221.56 - What are the requirements for transcription of the hearing?

Code of Federal Regulations, 2011 CFR

2011-10-01

... 50 Wildlife and Fisheries 9 2011-10-01 2011-10-01 false What are the requirements for transcription of the hearing? 221.56 Section 221.56 Wildlife and Fisheries NATIONAL MARINE FISHERIES SERVICE... requirements for transcription of the hearing? (a) Transcript and reporter's fees. The hearing will be...

Disruption of nucleotide excision repair by the human T-cell leukemia virus type 1 Tax protein.

PubMed

Kao, S Y; Marriott, S J

1999-05-01

The Tax protein of human T-cell leukemia virus type 1 (HTLV-1) is a transcriptional transactivator and viral oncogene. Since cellular transformation has been frequently linked to alterations in genome stability, we investigated the effect of Tax on nucleotide excision repair (NER), a prominent cellular DNA repair pathway. Cells expressing Tax exhibited a reduced capacity for NER as measured by unscheduled DNA synthesis and host cell reactivation assays. The cellular proliferating cell nuclear antigen (PCNA) gene product regulates DNA replication and repair pathways, including NER. Since Tax activates transcription of the PCNA promoter, we investigated whether this activity contributes to the reduction of NER. Tax increased endogenous PCNA protein expression, and analysis of Tax mutant proteins demonstrated that the reduction in NER correlated with Tax transactivation of PCNA gene expression. Direct overexpression of PCNA also reduced NER. We propose that overexpression of PCNA, and disruption of NER induced by Tax, predisposes cells to accumulate DNA damage and contributes to HTLV-1 transformation.

Ubiquitination and sumoylation of the HTLV-2 Tax-2B protein regulate its NF-κB activity: a comparative study with the HTLV-1 Tax-1 protein

PubMed Central

2012-01-01

Background Retroviruses HTLV-1 and HTLV-2 have homologous genomic structures but differ significantly in pathogenicity. HTLV-1 is associated with Adult T cell Leukemia (ATL), whereas infection by HTLV-2 has no association with neoplasia. Transformation of T lymphocytes by HTLV-1 is linked to the capacity of its oncoprotein Tax-1 to alter cell survival and cell cycle control mechanisms. Among these functions, Tax-1-mediated activation of cellular gene expression via the NF-κB pathway depends on Tax-1 post-translational modifications by ubiquitination and sumoylation. The Tax-2 protein of HTLV-2B (Tax-2B) is also modified by ubiquitination and sumoylation and activates the NF-κB pathway to a level similar to that of Tax-1. The present study aims to understand whether ubiquitination and sumoylation modifications are involved in Tax-2B-mediated activation of the NF-κB pathway. Results The comparison of Tax-1 and Tax-2B lysine to arginine substitution mutants revealed conserved patterns and levels of ubiquitination with notable difference in the lysine usage for sumoylation. Neither Tax-1 nor Tax-2B ubiquitination and sumoylation deficient mutants could activate the NF-κB pathway and fusion of ubiquitin or SUMO-1 to the C-terminus of the ubiquitination and sumoylation deficient Tax-2B mutant strikingly restored transcriptional activity. In addition, ubiquitinated forms of Tax-2B colocalized with RelA and IKKγ in prominent cytoplasmic structures associated with the Golgi apparatus, whereas colocalization of Tax-2B with the RelA subunit of NF-κB and the transcriptional coactivator p300 in punctate nuclear structures was dependent on Tax-2B sumoylation, as previously observed for Tax-1. Conclusions Both Tax-1 and Tax-2 activate the NF-κB pathway via similar mechanisms involving ubiquitination and sumoylation. Therefore, the different transforming potential of HTLV-1 and HTLV-2 is unlikely to be related to different modes of activation of the canonical NF-κB pathway

43 CFR 45.56 - What are the requirements for transcription of the hearing?

Code of Federal Regulations, 2010 CFR

2010-10-01

... 43 Public Lands: Interior 1 2010-10-01 2010-10-01 false What are the requirements for transcription of the hearing? 45.56 Section 45.56 Public Lands: Interior Office of the Secretary of the Interior....56 What are the requirements for transcription of the hearing? (a) Transcript and reporter's fees...

43 CFR 45.56 - What are the requirements for transcription of the hearing?

Code of Federal Regulations, 2011 CFR

2011-10-01

... 43 Public Lands: Interior 1 2011-10-01 2011-10-01 false What are the requirements for transcription of the hearing? 45.56 Section 45.56 Public Lands: Interior Office of the Secretary of the Interior....56 What are the requirements for transcription of the hearing? (a) Transcript and reporter's fees...

26 CFR 1.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 13 2010-04-01 2010-04-01 false Required use of magnetic media for corporate... Required use of magnetic media for corporate income tax returns. The return of a corporation that is required to be filed on magnetic media under § 301.6011-5 of this chapter must be filed in accordance with...

26 CFR 1.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2013 CFR

2013-04-01

... 26 Internal Revenue 13 2013-04-01 2013-04-01 false Required use of magnetic media for corporate....6011-5 Required use of magnetic media for corporate income tax returns. The return of a corporation that is required to be filed on magnetic media under § 301.6011-5 of this chapter must be filed in...

26 CFR 1.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2012 CFR

2012-04-01

... 26 Internal Revenue 13 2012-04-01 2012-04-01 false Required use of magnetic media for corporate....6011-5 Required use of magnetic media for corporate income tax returns. The return of a corporation that is required to be filed on magnetic media under § 301.6011-5 of this chapter must be filed in...

26 CFR 1.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 13 2011-04-01 2011-04-01 false Required use of magnetic media for corporate....6011-5 Required use of magnetic media for corporate income tax returns. The return of a corporation that is required to be filed on magnetic media under § 301.6011-5 of this chapter must be filed in...

26 CFR 1.6011-5 - Required use of magnetic media for corporate income tax returns.

Code of Federal Regulations, 2014 CFR

2014-04-01

... 26 Internal Revenue 13 2014-04-01 2014-04-01 false Required use of magnetic media for corporate....6011-5 Required use of magnetic media for corporate income tax returns. The return of a corporation that is required to be filed on magnetic media under § 301.6011-5 of this chapter must be filed in...

Tax-exempts feeling the heat.

PubMed

Greene, J

1995-11-20

Should government change decades-old tax codes to require that not-for-profit hospitals prove they deserve their tax exemptions? Healthcare Corp. has suggested that tax codes be re-examined because some not-for-profits provide less charity care than the value of their tax exemptions.

Mechanism of DNA-binding enhancement by the human T-cell leukaemia virus transactivator Tax.

PubMed

Baranger, A M; Palmer, C R; Hamm, M K; Giebler, H A; Brauweiler, A; Nyborg, J K; Schepartz, A

1995-08-17

Tax protein activates transcription of the human T-cell leukaemia virus type I (HTLV-I) genome through three imperfect cyclic AMP-responsive element (CRE) target sites located within the viral promoter. Previous work has shown that Tax interacts with the bZIP element of proteins that bind the CRE target site to promote peptide dimerization, suggesting an association between Tax and bZIP coiled coil. Here we show that the site of interaction with Tax is not the coiled coil, but the basic segment. This interaction increases the stability of the GCN4 bZIP dimer by 1.7 kcal mol-1 and the DNA affinity of the dimer by 1.9 kcal mol-1. The differential effect of Tax on several bZip-DNA complexes that differ in peptide sequence or DNA conformation suggests a model for Tax action based on stabilization of a distinct DNA-bound protein structure. This model may explain how Tax interacts with transcription factors of considerable sequence diversity to alter patterns of gene expression.

HTLV-I Tax and cell cycle progression.

PubMed

Neuveut, C; Jeang, K T

2000-01-01

Human T-cell leukemia virus type I (HTLV-I) is the etiological agent for adult T-cell leukemia (ATL) and various human myopathies/neuropathies. HTLV-I encodes a 40 kDa phosphoprotein, Tax, which has been implicated in cellular transformation. In similarity with several other oncoproteins such as Myc, Jun, and Fos, Tax is a transcriptional activator. How Tax mechanistically dysregulates the cell cycle remains unclear. Recent findings from us and others have shown that Tax targets key regulators of G1/S and M progression such as p16INK4a, cyclin D1, cyclin D3-cdk, and the mitotic spindle checkpoint apparatus. Thus, Tax influences the progression of cells in various phases of the cell cycle. In this regard, we will discuss three distinct mechanisms through which Tax affects cell-cycling: a) through direct association Tax can abrogate the inhibitory function of p16INK4a on the G1-cdks, b) Tax can also directly influence cyclin D-cdk activities by a protein-protein interaction, and c) Tax targets the HsMAD1 mitotic spindle-assembly checkpoint protein. Through these varied routes, the HTLV-I oncoprotein dysregulates cellular growth controls and engenders a proclivity of cells toward a loss of DNA-damage surveillance.

Tax-1 and Tax-2 similarities and differences: focus on post-translational modifications and NF-κB activation

PubMed Central

Shirinian, Margret; Kfoury, Youmna; Dassouki, Zeina; El-Hajj, Hiba; Bazarbachi, Ali

2013-01-01

Although human T cell leukemia virus type 1 and 2 (HTLV-1 and HTLV-2) share similar genetic organization, they have major differences in their pathogenesis and disease manifestation. HTLV-1 is capable of transforming T lymphocytes in infected patients resulting in adult T cell leukemia/lymphoma whereas HTLV-2 is not clearly associated with lymphoproliferative diseases. Numerous studies have provided accumulating evidence on the involvement of the viral transactivators Tax-1 versus Tax-2 in T cell transformation. Tax-1 is a potent transcriptional activator of both viral and cellular genes. Tax-1 post-translational modifications and specifically ubiquitylation and SUMOylation have been implicated in nuclear factor-kappaB (NF-κB) activation and may contribute to its transformation capacity. Although Tax-2 has similar protein structure compared to Tax-1, the two proteins display differences both in their protein–protein interaction and activation of signal transduction pathways. Recent studies on Tax-2 have suggested ubiquitylation and SUMOylation independent mechanisms of NF-κB activation. In this present review, structural and functional differences between Tax-1 and Tax-2 will be summarized. Specifically, we will address their subcellular localization, nuclear trafficking and their effect on cellular regulatory proteins. A special attention will be given to Tax-1/Tax-2 post-translational modification such as ubiquitylation, SUMOylation, phosphorylation, acetylation, NF-κB activation, and protein–protein interactions involved in oncogenecity both in vivo and in vitro. PMID:23966989

26 CFR 31.6302(c)-3 - Deposit rules for taxes under the Federal Unemployment Tax Act.

Code of Federal Regulations, 2012 CFR

2012-04-01

... Unemployment Tax Act. 31.6302(c)-3 Section 31.6302(c)-3 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT... for taxes under the Federal Unemployment Tax Act. (a) Requirement—(1) In general. Except as provided... deposit. For the requirement to deposit tax under the Federal Unemployment Tax Act by electronic funds...

26 CFR 31.6302(c)-3 - Deposit rules for taxes under the Federal Unemployment Tax Act.

Code of Federal Regulations, 2013 CFR

2013-04-01

... Unemployment Tax Act. 31.6302(c)-3 Section 31.6302(c)-3 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT... for taxes under the Federal Unemployment Tax Act. (a) Requirement—(1) In general. Except as provided... deposit. For the requirement to deposit tax under the Federal Unemployment Tax Act by electronic funds...

26 CFR 31.6302(c)-3 - Deposit rules for taxes under the Federal Unemployment Tax Act.

Code of Federal Regulations, 2014 CFR

2014-04-01

... Unemployment Tax Act. 31.6302(c)-3 Section 31.6302(c)-3 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT... for taxes under the Federal Unemployment Tax Act. (a) Requirement—(1) In general. Except as provided... deposit. For the requirement to deposit tax under the Federal Unemployment Tax Act by electronic funds...

26 CFR 31.6302(c)-3 - Deposit rules for taxes under the Federal Unemployment Tax Act.

Code of Federal Regulations, 2011 CFR

2011-04-01

... Unemployment Tax Act. 31.6302(c)-3 Section 31.6302(c)-3 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT... for taxes under the Federal Unemployment Tax Act. (a) Requirement—(1) In general. Except as provided... deposit. For the requirement to deposit tax under the Federal Unemployment Tax Act by electronic funds...

Human T-cell leukemia virus type 1 Tax requires direct access to DNA for recruitment of CREB binding protein to the viral promoter.

PubMed

Lenzmeier, B A; Giebler, H A; Nyborg, J K

1998-02-01

Efficient human T-cell leukemia virus type 1 (HTLV-1) replication and viral gene expression are dependent upon the virally encoded oncoprotein Tax. To activate HTLV-1 transcription, Tax interacts with the cellular DNA binding protein cyclic AMP-responsive element binding protein (CREB) and recruits the coactivator CREB binding protein (CBP), forming a nucleoprotein complex on the three viral cyclic AMP-responsive elements (CREs) in the HTLV-1 promoter. Short stretches of dG-dC-rich (GC-rich) DNA, immediately flanking each of the viral CREs, are essential for Tax recruitment of CBP in vitro and Tax transactivation in vivo. Although the importance of the viral CRE-flanking sequences is well established, several studies have failed to identify an interaction between Tax and the DNA. The mechanistic role of the viral CRE-flanking sequences has therefore remained enigmatic. In this study, we used high resolution methidiumpropyl-EDTA iron(II) footprinting to show that Tax extended the CREB footprint into the GC-rich DNA flanking sequences of the viral CRE. The Tax-CREB footprint was enhanced but not extended by the KIX domain of CBP, suggesting that the coactivator increased the stability of the nucleoprotein complex. Conversely, the footprint pattern of CREB on a cellular CRE lacking GC-rich flanking sequences did not change in the presence of Tax or Tax plus KIX. The minor-groove DNA binding drug chromomycin A3 bound to the GC-rich flanking sequences and inhibited the association of Tax and the Tax-CBP complex without affecting CREB binding. Tax specifically cross-linked to the viral CRE in the 5'-flanking sequence, and this cross-link was blocked by chromomycin A3. Together, these data support a model where Tax interacts directly with both CREB and the minor-groove viral CRE-flanking sequences to form a high-affinity binding site for the recruitment of CBP to the HTLV-1 promoter.

New tax laws require slight shifts in hospitals' funding strategies.

PubMed

Bromberg, R S

1979-07-16

Recent tax laws that affect hospitals' deferred compensation plans, employment taxes, annuities, foundation grants, unrelated business income, and gifts of appreciated property will not seriously affect charitable giving to hospitals.

Move or Die: the Fate of the Tax Oncoprotein of HTLV-1

PubMed Central

Lodewick, Julie; Lamsoul, Isabelle; Bex, Françoise

2011-01-01

The HTLV-1 Tax protein both activates viral replication and is involved in HTLV-1-mediated transformation of T lymphocytes. The transforming properties of Tax include altering the expression of select cellular genes via activation of cellular pathways and perturbation of both cell cycle control mechanisms and apoptotic signals. The recent discovery that Tax undergoes a hierarchical sequence of posttranslational modifications that control its intracellular localization provides provocative insights into the mechanisms regulating Tax transcriptional and transforming activities. PMID:21994756

Regulation of the tumor marker Fascin by the viral oncoprotein Tax of human T-cell leukemia virus type 1 (HTLV-1) depends on promoter activation and on a promoter-independent mechanism.

PubMed

Mohr, Caroline F; Gross, Christine; Bros, Matthias; Reske-Kunz, Angelika B; Biesinger, Brigitte; Thoma-Kress, Andrea K

2015-11-01

Adult T-cell leukemia/lymphoma is a highly infiltrative neoplasia of CD4(+) T-lymphocytes that occurs in about 5% of carriers infected with the deltaretrovirus human T-cell leukemia virus type 1 (HTLV-1). The viral oncoprotein Tax perturbs cellular signaling pathways leading to upregulation of host cell factors, amongst them the actin-bundling protein Fascin, an invasion marker of several types of cancer. However, transcriptional regulation of Fascin by Tax is poorly understood. In this study, we identified a triple mode of transcriptional induction of Fascin by Tax, which requires (1) NF-κB-dependent promoter activation, (2) a Tax-responsive region in the Fascin promoter, and (3) a promoter-independent mechanism sensitive to the Src family kinase inhibitor PP2. Thus, Tax regulates Fascin by a multitude of signals. Beyond, using Tax-expressing and virus-transformed lymphocytes as a model system, our study is the first to identify the invasion marker Fascin as a novel target of PP2, an inhibitor of metastasis. Copyright © 2015 Elsevier Inc. All rights reserved.

Transcriptional requirements of the distal heavy-strand promoter of mtDNA

PubMed Central

Zollo, Ornella; Tiranti, Valeria; Sondheimer, Neal

2012-01-01

The heavy strand of mtDNA contains two promoters with nonoverlapping functions. The role of the minor heavy-strand promoter (HSP2) is controversial, because the promoter has been difficult to activate in an in vitro system. We have isolated HSP2 by excluding its interaction with the more powerful HSP1 promoter, and we find that it is transcribed efficiently by recombinant mtRNA polymerase and mitochondrial transcription factor B2. The mitochondrial transcription factor A is not required for initiation, but it has the ability to alternatively activate and repress the HSP2 transcriptional unit depending on the ratio between mitochondrial transcription factor A and other transcription factors. The positioning of transcriptional initiation agrees with our current understanding of HSP2 activity in vivo. Serial deletion of HSP2 shows that only proximal sequences are required. Several mutations, including the disruption of a polycytosine track upstream of the HSP2 initiation site, influence transcriptional activity. Transcription from HSP2 is also observed when HeLa cell mitochondrial extract is used as the source of mitochondrial polymerase, and this transcription is maintained when HSP2 is provided in proper spacing and context to the HSP1 promoter. Studies of the linked heavy-strand promoters show that they are differentially regulated by ATP dosage. We conclude that HSP2 is transcribed and has features that allow it to regulate mitochondrial mRNA synthesis. PMID:22454497

The HTLV-1 oncoprotein Tax is modified by the ubiquitin related modifier 1 (Urm1).

PubMed

Hleihel, Rita; Khoshnood, Behzad; Dacklin, Ingrid; Omran, Hayssam; Mouawad, Carine; Dassouki, Zeina; El-Sabban, Marwan; Shirinian, Margret; Grabbe, Caroline; Bazarbachi, Ali

2018-04-17

Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy secondary to chronic human T-cell lymphotropic virus 1 infection, triggered by the virally encoded oncoprotein Tax. The transforming activity and subcellular localization of Tax is strongly influenced by posttranslational modifications, among which ubiquitylation and SUMOylation have been identified as key regulators of the nuclear/cytoplasmic shuttling of Tax, as well as its ability to activate NF-κB signaling. Adding to the complex posttranslational modification landscape of Tax, we here demonstrate that Tax also interacts with the ubiquitin-related modifier 1 (Urm1). Conjugation of Urm1 to Tax results in a redistribution of Tax to the cytoplasm and major increase in the transcription of the NF-ĸB targets Rantes and interleukin-6. Utilizing a tax-transgenic Drosophila model, we show that the Urm1-dependent subcellular targeting of Tax is evolutionary conserved, and that the presence of Urm1 is strongly correlated with the transcriptional output of Diptericin, an antimicrobial peptide and established downstream target of NF-κB in flies. These data put forward Urm1 as a novel Tax modifier that modulates its oncogenic activity and hence represents a potential novel target for developing new strategies for treating ATL.

The Interaction Between Tax and Expenditure Limitations, Supermajority Requirements, and School Finance Litigation

ERIC Educational Resources Information Center

Jordan, Teresa S.; Jordan, K. Forbis; Crawford, James

2005-01-01

This article focuses on the change in selected state-level school finance variables from 1970 to 2000, with particular attention to the changes in these variables and school finance litigation decisions in states with and without state-level tax and expenditure limitations (TELs) or supermajority requirements (SMRs). The magnitude of the decrease…

Dissecting protein:protein interactions between transcription factors with an RNA aptamer.

PubMed Central

Tian, Y; Adya, N; Wagner, S; Giam, C Z; Green, M R; Ellington, A D

1995-01-01

Nucleic acid aptamers isolated from random sequence pools have generally proven useful at inhibiting the interactions of nucleic acid binding proteins with their cognate nucleic acids. In order to develop reagents that could also be used to study protein:protein interactions, we have used in vitro selection to search for RNA aptamers that could interact with the transactivating protein Tax from human T-cell leukemia virus. Tax does not normally bind to nucleic acids, but instead stimulates transcription by interacting with a variety of cellular transcription factors, including the cyclic AMP-response element binding protein (CREB), NF-kappa B, and the serum response factor (SRF). Starting from a pool of greater than 10(13) different RNAs with a core of 120 random sequence positions, RNAs were selected for their ability to be co-retained on nitrocellulose filters with Tax. After five cycles of selection and amplification, a single nucleic acid species remained. This aptamer was found to bind Tax with high affinity and specificity, and could disrupt complex formation between Tax and NF-kappa B, but not with SRF. The differential effects of our aptamer probe on protein:protein interactions suggest a model for how the transcription factor binding sites on the surface of the Tax protein are organized. This model is consistent with data from a variety of other studies. PMID:7489503

Lethal cutaneous disease in transgenic mice conditionally expressing type I human T cell leukemia virus Tax.

PubMed

Kwon, Hakju; Ogle, Louise; Benitez, Bobby; Bohuslav, Jan; Montano, Mauricio; Felsher, Dean W; Greene, Warner C

2005-10-21

Type I human T cell leukemia virus (HTLV-I) is etiologically linked with adult T cell leukemia, an aggressive and usually fatal expansion of activated CD4+ T lymphocytes that frequently traffic to skin. T cell transformation induced by HTLV-I involves the action of the 40-kDa viral Tax transactivator protein. Tax both stimulates the HTLV-I long terminal repeat and deregulates the expression of select cellular genes by altering the activity of specific host transcription factors, including cyclic AMP-responsive element-binding protein (CREB)/activating transcription factor, NF-kappaB/Rel, and serum response factor. To study initiating events involved in HTLV-I Tax-induced T cell transformation, we generated "Tet-off" transgenic mice conditionally expressing in a lymphocyte-restricted manner (EmuSR alpha promoter-enhancer) either wild-type Tax or mutant forms of Tax that selectively compromise the NF-kappaB (M22) or CREB/activating transcription factor (M47) activation pathways. Wild-type Tax and M47 Tax-expressing mice, but not M22-Tax expressing mice, developed progressive alopecia, hyperkeratosis, and skin lesions containing profuse activated CD4 T cell infiltrates with evidence of deregulated inflammatory cytokine production. In addition, these animals displayed systemic lymphadenopathy and splenomegaly. These findings suggest that Tax-mediated activation of NF-kappaB plays a key role in the development of this aggressive skin disease that shares several features in common with the skin disease occurring during the preleukemic stage in HTLV-I-infected patients. Of note, this skin disease completely resolved when Tax transgene expression was suppressed by administration of doxycycline, emphasizing the key role played by this viral oncoprotein in the observed pathology.

Permissive Sense and Antisense Transcription from the 5′ and 3′ Long Terminal Repeats of Human T-Cell Leukemia Virus Type 1

PubMed Central

Polakowski, Nicholas; Hoang, Kimson

2016-01-01

ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus, and, as such, its genome becomes chromosomally integrated following infection. The resulting provirus contains identical 5′ and 3′ peripheral long terminal repeats (LTRs) containing bidirectional promoters. Antisense transcription from the 3′ LTR regulates expression of a single gene, hbz, while sense transcription from the 5′ LTR controls expression of all other viral genes, including tax. Both the HBZ and Tax proteins are implicated in the development of adult T-cell leukemia (ATL), a T-cell malignancy caused by HTLV-1 infection. However, these proteins appear to harbor opposing molecular functions, indicating that they may act independently and at different time points prior to leukemogenesis. Here, we used bidirectional reporter constructs to test whether transcriptional interference serves as a mechanism that inhibits simultaneous expression of Tax and HBZ. We found that sense transcription did not interfere with antisense transcription from the 3′ LTR and vice versa, even with strong transcription emanating from the opposing direction. Therefore, bidirectional transcription across the provirus might not restrict hbz or tax expression. Single-cell analyses revealed that antisense transcription predominates in the absence of Tax, which transactivates viral sense transcription. Interestingly, a population of Tax-expressing cells exhibited antisense but not activated sense transcription. Consistent with the ability of Tax to induce cell cycle arrest, this population was arrested in G0/G1 phase. These results imply that cell cycle arrest inhibits Tax-mediated activation of sense transcription without affecting antisense transcription, which may be important for long-term viral latency. IMPORTANCE The chromosomally integrated form of the retrovirus human T-cell leukemia virus type 1 (HTLV-1) contains identical DNA sequences, known as long terminal repeats (LTRs), at its 5′ and 3�

Human T-cell leukemia virus type I oncoprotein Tax represses Smad-dependent transforming growth factor beta signaling through interaction with CREB-binding protein/p300.

PubMed

Mori, N; Morishita, M; Tsukazaki, T; Giam, C Z; Kumatori, A; Tanaka, Y; Yamamoto, N

2001-04-01

Human T-cell leukemia virus type I (HTLV-I) Tax is a potent transcriptional regulator that can activate or repress specific cellular genes and that has been proposed to contribute to leukemogenesis in adult T-cell leukemia. Previously, HTLV-I- infected T-cell clones were found to be resistant to growth inhibition by transforming growth factor (TGF)-beta. Here it is shown that Tax can perturb Smad-dependent TGF-beta signaling even though no direct interaction of Tax and Smad proteins could be detected. Importantly, a mutant Tax of CREB-binding protein (CBP)/p300 binding site, could not repress the Smad transactivation function, suggesting that the CBP/p300 binding domain of Tax is essential for the suppression of Smad function. Because both Tax and Smad are known to interact with CBP/p300 for the potentiation of their transcriptional activities, the effect of CBP/p300 on suppression of Smad-mediated transactivation by Tax was examined. Overexpression of CBP/p300 reversed Tax-mediated inhibition of Smad transactivation. Furthermore, Smad could repress Tax transcriptional activation, indicating reciprocal repression between Tax and Smad. These results suggest that Tax interferes with the recruitment of CBP/p300 into transcription initiation complexes on TGF-beta-responsive elements through its binding to CBP/p300. The novel function of Tax as a repressor of TGF-beta signaling may contribute to HTLV-I leukemogenesis. (Blood. 2001;97:2137-2144)

IRS issues guidance on tax-exempt bond requirements.

PubMed

Kalick, L

1998-07-01

Enforcing compliance with rules governing facilities financed with tax-exempt bonds recently has become an IRS priority. Integrated delivery systems (IDSs) that include such facilities, therefore, should take steps to ensure that the private business use of those facilities does not exceed the legal threshold amount, thereby jeopardizing the tax-exempt status of the bonds. Management contracts, research agreements, and leases are arrangements with the greatest potential to result in noncompliance. Instituting a compliance program to monitor the use of bond proceeds and minimize the amount of private business use of facilities over the bond term can reduce an organization's risk of penalty.

The nuclear import of the human T lymphotropic virus type I (HTLV-1) tax protein is carrier- and energy-independent.

PubMed

Tsuji, Takahiro; Sheehy, Noreen; Gautier, Virginie W; Hayakawa, Hitoshi; Sawa, Hirofumi; Hall, William W

2007-05-04

HTLV-1 is the etiologic agent of the adult T cell leukemialymphoma (ATLL). The viral regulatory protein Tax plays a central role in leukemogenesis as a transcriptional transactivator of both viral and cellular gene expression, and this requires Tax activity in both the cytoplasm and the nucleus. In the present study, we have investigated the mechanisms involved in the nuclear localization of Tax. Employing a GFP fusion expression system and a range of Tax mutants, we could confirm that the N-terminal 60 amino acids, and specifically residues within the zinc finger motif in this region, are important for nuclear localization. Using an in vitro nuclear import assay, it could be demonstrated that the transportation of Tax to the nucleus required neither energy nor carrier proteins. Specific and direct binding between Tax and p62, a nucleoporin with which the importin beta family of proteins have been known to interact was also observed. The nuclear import activity of wild type Tax and its mutants and their binding affinity for p62 were also clearly correlated, suggesting that the entry of Tax into the nucleus involves a direct interaction with nucleoporins within the nuclear pore complex (NPC). The nuclear export of Tax was also shown to be carrier independent. It could be also demonstrated that Tax it self may have a carrier function and that the NF-kappaB subunit p65 could be imported into the nucleus by Tax. These studies suggest that Tax could alter the nucleocytoplasmic distribution of cellular proteins, and this could contribute to the deregulation of cellular processes observed in HTLV-1 infection.

BCL11B is frequently downregulated in HTLV-1-infected T-cells through Tax-mediated proteasomal degradation.

PubMed

Permatasari, Happy Kurnia; Nakahata, Shingo; Ichikawa, Tomonaga; Morishita, Kazuhiro

2017-08-26

Human T-cell leukemia virus type 1 (HTLV-1) is a causative agent of adult T-cell leukemia-lymphoma (ATLL). The HTLV-1-encoded protein Tax plays important roles in the proliferation of HTLV-1-infected T-cells by affecting cellular proteins. In this study, we showed that Tax transcriptionally and post-transcriptionally downregulates the expression of the tumor suppressor gene B-cell leukemia/lymphoma 11B (BCL11B), which encodes a lymphoid-related transcription factor. BCL11B expression was downregulated in HTLV-1-infected T-cell lines at the mRNA and protein levels, and forced expression of BCL11B suppressed the proliferation of these cells. The proteasomal inhibitor MG132 increased BCL11B expression in HTLV-1-infected cell lines, and colocalization of Tax with BCL11B was detected in the cytoplasm of HTLV-1-infected T-cells following MG132 treatment. shRNA knock-down of Tax expression also increased the expression of BCL11B in HTLV-1-infected cells. Moreover, we found that Tax physically binds to BCL11B protein and induces the polyubiquitination of BCL11B and proteasome-dependent degradation of BCL11B. Thus, inactivation of BCL11B by Tax protein may play an important role in the Tax-mediated leukemogenesis. Copyright © 2017 Elsevier Inc. All rights reserved.

SIRT1 Suppresses Human T-Cell Leukemia Virus Type 1 Transcription

PubMed Central

Tang, Hei-Man Vincent; Gao, Wei-Wei; Chan, Chi-Ping; Cheng, Yun; Deng, Jian-Jun; Yuen, Kit-San; Iha, Hidekatsu

2015-01-01

ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1)-associated diseases are poorly treatable, and HTLV-1 vaccines are not available. High proviral load is one major risk factor for disease development. HTLV-1 encodes Tax oncoprotein, which activates transcription from viral long terminal repeats (LTR) and various types of cellular promoters. Counteracting Tax function might have prophylactic and therapeutic benefits. In this work, we report on the suppression of Tax activation of HTLV-1 LTR by SIRT1 deacetylase. The transcriptional activity of Tax on the LTR was largely ablated when SIRT1 was overexpressed, but Tax activation of NF-κB was unaffected. On the contrary, the activation of the LTR by Tax was boosted when SIRT1 was depleted. Treatment of cells with resveratrol shunted Tax activity in a SIRT1-dependent manner. The activation of SIRT1 in HTLV-1-transformed T cells by resveratrol potently inhibited HTLV-1 proviral transcription and Tax expression, whereas compromising SIRT1 by specific inhibitors augmented HTLV-1 mRNA expression. The administration of resveratrol also decreased the production of cell-free HTLV-1 virions from MT2 cells and the transmission of HTLV-1 from MT2 cells to uninfected Jurkat cells in coculture. SIRT1 associated with Tax in HTLV-1-transformed T cells. Treatment with resveratrol prevented the interaction of Tax with CREB and the recruitment of CREB, CRTC1, and p300 to Tax-responsive elements in the LTR. Our work demonstrates the negative regulatory function of SIRT1 in Tax activation of HTLV-1 transcription. Small-molecule activators of SIRT1 such as resveratrol might be considered new prophylactic and therapeutic agents in HTLV-1-associated diseases. IMPORTANCE Human T-cell leukemia virus type 1 (HTLV-1) causes a highly lethal blood cancer or a chronic debilitating disease of the spinal cord. Treatments are unsatisfactory, and vaccines are not available. Disease progression is associated with robust expression of HTLV-1 genes

76 FR 66181 - Disregarded Entities; Excise Taxes and Employment Taxes

Federal Register 2010, 2011, 2012, 2013, 2014

2011-10-26

... particular, disregarded entities that pay or pay over certain federal excise taxes or that are required to be... assessed against Z and, in the event that Z fails to pay the liability after notice and demand, a general...)(C) Example (i) and (ii) of this section. If LLCB does not pay the tax on its sale of coal under...

Regulatory elements involved in tax-mediated transactivation of the HTLV-I LTR.

PubMed

Seeler, J S; Muchardt, C; Podar, M; Gaynor, R B

1993-10-01

HTLV-I is the etiologic agent of adult T-cell leukemia. In this study, we investigated the regulatory elements and cellular transcription factors which function in modulating HTLV-I gene expression in response to the viral transactivator protein, tax. Transfection experiments into Jurkat cells of a variety of site-directed mutants in the HTLV-1 LTR indicated that each of the three motifs A, B, and C within the 21-bp repeats, the binding sites for the Ets family of proteins, and the TATA box all influenced the degree of tax-mediated activation. Tax is also able to activate gene expression of other viral and cellular promoters. Tax activation of the IL-2 receptor and the HIV-1 LTR is mediated through NF-kappa B motifs. Interestingly, sequences in the 21-bp repeat B and C motifs contain significant homology with NF-kappa B regulatory elements. We demonstrated that an NF-kappa B binding protein, PRDII-BF1, but not the rel protein, bound to the B and C motifs in the 21-bp repeat. PRDII-BF1 was also able to stimulate activation of HTLV-I gene expression by tax. The role of the Ets proteins on modulating tax activation was also studied. Ets 1 but not Ets 2 was capable of increasing the degree of tax activation of the HTLV-I LTR. These results suggest that tax activates gene expression by either direct or indirect interaction with several cellular transcription factors that bind to the HTLV-I LTR.

26 CFR 31.6302(c)-3 - Use of Government depositaries in connection with tax under the Federal Unemployment Tax Act.

Code of Federal Regulations, 2010 CFR

2010-04-01

... with tax under the Federal Unemployment Tax Act. 31.6302(c)-3 Section 31.6302(c)-3 Internal Revenue...) § 31.6302(c)-3 Use of Government depositaries in connection with tax under the Federal Unemployment Tax... transfer. For the requirement to deposit tax under the Federal Unemployment Tax Act by electronic funds...

Enhancer Activation Requires Trans-Recruitment of a Mega Transcription Factor Complex

PubMed Central

Liu, Zhijie; Merkurjev, Daria; Yang, Feng; Li, Wenbo; Oh, Soohwan; Friedman, Meyer J.; Song, Xiaoyuan; Zhang, Feng; Ma, Qi; Ohgi, Kenneth; Krones, Anna; Rosenfeld, Michael G.

2014-01-01

Summary Enhancers provide critical information directing cell-type specific transcriptional programs, regulated by binding of signal-dependent transcription factors and their associated cofactors. Here we report that the most strongly activated estrogen (E2)-responsive enhancers are characterized by trans-recruitment and in situ assembly of a large 1-2 MDa complex of diverse DNA-binding transcription factors by ERα at ERE-containing enhancers. We refer to enhancers recruiting these factors as mega transcription factor-bound in trans (MegaTrans) enhancers. The MegaTrans complex is a signature of the most potent functional enhancers and is required for activation of enhancer RNA transcription and recruitment of coactivators, including p300 and Med1. The MegaTrans complex functions, in part, by recruiting specific enzymatic machinery, exemplified by DNA-dependent protein kinase. Thus, MegaTrans-containing enhancers represent a cohort of functional enhancers that mediate a broad and important transcriptional program and provide a molecular explanation for transcription factor clustering and hotspots noted in the genome. PMID:25303530

Montana fuel tax refunds : draft final report.

DOT National Transportation Integrated Search

2011-11-01

"The primary source of funding for transportation infrastructure is the taxes that are imposed on motor fuels. One aspect of fuel tax collections is the process that requires consumers to apply for refunds of taxes paid on fuels used for tax-exempt p...

48 CFR 2929.101 - Resolving tax problems.

Code of Federal Regulations, 2010 CFR

2010-10-01

... 48 Federal Acquisition Regulations System 7 2010-10-01 2010-10-01 false Resolving tax problems. 2929.101 Section 2929.101 Federal Acquisition Regulations System DEPARTMENT OF LABOR GENERAL CONTRACTING REQUIREMENTS TAXES General 2929.101 Resolving tax problems. Contract tax problems or questions...

48 CFR 1329.101 - Resolving tax problems.

Code of Federal Regulations, 2010 CFR

2010-10-01

... 48 Federal Acquisition Regulations System 5 2010-10-01 2010-10-01 false Resolving tax problems. 1329.101 Section 1329.101 Federal Acquisition Regulations System DEPARTMENT OF COMMERCE GENERAL CONTRACTING REQUIREMENTS TAXES General 1329.101 Resolving tax problems. Legal questions relating to tax issues...

48 CFR 629.101 - Resolving tax problems.

Code of Federal Regulations, 2010 CFR

2010-10-01

... 48 Federal Acquisition Regulations System 4 2010-10-01 2010-10-01 false Resolving tax problems... REQUIREMENTS TAXES General 629.101 Resolving tax problems. In certain instances, acquisitions by posts are exempt from various taxes in foreign countries. Contracting officers shall ascertain such exemptions and...

7 CFR 1.656 - What are the requirements for transcription of the hearing?

Code of Federal Regulations, 2011 CFR

2011-01-01

... 7 Agriculture 1 2011-01-01 2011-01-01 false What are the requirements for transcription of the hearing? 1.656 Section 1.656 Agriculture Office of the Secretary of Agriculture ADMINISTRATIVE REGULATIONS... transcription of the hearing? (a) Transcript and reporter's fees. The hearing will be transcribed verbatim. (1...

7 CFR 1.656 - What are the requirements for transcription of the hearing?

Code of Federal Regulations, 2010 CFR

2010-01-01

... 7 Agriculture 1 2010-01-01 2010-01-01 false What are the requirements for transcription of the hearing? 1.656 Section 1.656 Agriculture Office of the Secretary of Agriculture ADMINISTRATIVE REGULATIONS... transcription of the hearing? (a) Transcript and reporter's fees. The hearing will be transcribed verbatim. (1...

48 CFR 2429.101 - Resolving tax problems.

Code of Federal Regulations, 2010 CFR

2010-10-01

... DEVELOPMENT GENERAL CONTRACTING REQUIREMENTS TAXES General 2429.101 Resolving tax problems. In order to have uniformity in HUD's treatment of the tax aspects of contracting and ensure effective cooperation with other... within HUD for handling all those tax problems. Therefore, the contracting activity will not engage in...

48 CFR 29.101 - Resolving tax problems.

Code of Federal Regulations, 2010 CFR

2010-10-01

.... (d) Before purchasing goods or services from a foreign source, the contracting officer should consult... 48 Federal Acquisition Regulations System 1 2010-10-01 2010-10-01 false Resolving tax problems. 29... CONTRACTING REQUIREMENTS TAXES General 29.101 Resolving tax problems. (a) Contract tax problems are...

48 CFR 229.101 - Resolving tax problems.

Code of Federal Regulations, 2011 CFR

2011-10-01

... 48 Federal Acquisition Regulations System 3 2011-10-01 2011-10-01 false Resolving tax problems..., DEPARTMENT OF DEFENSE GENERAL CONTRACTING REQUIREMENTS TAXES General 229.101 Resolving tax problems. (a... information on fuel excise taxes, see PGI 229.101(b). (c) For guidance on directing a contractor to litigate...

Energy taxes fought by industry

DOE Office of Scientific and Technical Information (OSTI.GOV)

Begley, R.

1993-02-10

Tax talk is heating up in Washington, and industry interests are beating the drum against any and all energy tax proposals. Without offering any details, Treasury Secretary Lloyd Bentsen has placed a broad-based energy tax on the table. American Petroleum Institute (API) president Charles J. DiBona says such a tax would damage the US economy just as it is beginning to recover. He acknowledges the deficit is a national problem, but says if any additional tax is required it should be a broad-based consumption tax such as a European-style value-added tax, a view shared by the Chemical Manufacturers Association (CMA).more » DiBona says taxes aimed only at energy would hurt consumers, damage the international competitiveness of US industry by raising energy prices, and raise the costs of doing business. National Association of Manufacturers president Jerry Jasinowski adds that broadbased energy taxes are really taxes on industrial production that will harm US made goods both at home and abroad.« less

48 CFR 31.205-41 - Taxes.

Code of Federal Regulations, 2011 CFR

2011-10-01

... 48 Federal Acquisition Regulations System 1 2011-10-01 2011-10-01 false Taxes. 31.205-41 Section... REQUIREMENTS CONTRACT COST PRINCIPLES AND PROCEDURES Contracts With Commercial Organizations 31.205-41 Taxes. (a) The following types of costs are allowable: (1) Federal, State, and local taxes (see part 29...

LKB1 tumor suppressor and salt-inducible kinases negatively regulate human T-cell leukemia virus type 1 transcription

PubMed Central

2013-01-01

Background Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL). Treatment options are limited and prophylactic agents are not available. We have previously demonstrated an essential role for CREB-regulating transcriptional coactivators (CRTCs) in HTLV-1 transcription. Results In this study we report on the negative regulatory role of LKB1 tumor suppressor and salt-inducible kinases (SIKs) in the activation of HTLV-1 long terminal repeats (LTR) by the oncoprotein Tax. Activation of LKB1 and SIKs effectively blunted Tax activity in a phosphorylation-dependent manner, whereas compromising these kinases, but not AMP-dependent protein kinases, augmented Tax function. Activated LKB1 and SIKs associated with Tax and suppressed Tax-induced LTR activation by counteracting CRTCs and CREB. Enforced expression of LKB1 or SIK1 in cells transfected with HTLV-1 molecular clone pX1MT repressed proviral transcription. On the contrary, depletion of LKB1 in pX1MT-transfected cells and in HTLV-1-transformed T cells boosted the expression of Tax. Treatment of HTLV-1 transformed cells with metformin led to LKB1/SIK1 activation, reduction in Tax expression, and inhibition of cell proliferation. Conclusions Our findings revealed a new function of LKB1 and SIKs as negative regulators of HTLV-1 transcription. Pharmaceutical activation of LKB1 and SIKs might be considered as a new strategy in anti-HTLV-1 and anti-ATL therapy. PMID:23577667

27 CFR 70.411 - Imposition of taxes, qualification requirements, and regulations.

Code of Federal Regulations, 2010 CFR

2010-04-01

... Provisions Relating to Distilled Spirits, Wines, and Beer § 70.411 Imposition of taxes, qualification... of 1954 imposes taxes on distilled spirits (including alcohol), wine and beer. (b) Qualification... to distilled spirits, wines, and beer which are within the jurisdiction of TTB are published in the...

76 FR 52862 - Time for Payment of Certain Excise Taxes, and Quarterly Excise Tax Payments for Small Alcohol...

Federal Register 2010, 2011, 2012, 2013, 2014

2011-08-24

... 40 Cigars and cigarettes, Claims, Electronic fund transfers, Excise taxes, Labeling, Packaging and... that are not required to pay taxes through electronic funds transfer (EFT), this first payment period..., Electronic funds transfers, Excise taxes, Exports, Food additives, Fruit juices, Labeling, Liquors, Packaging...

The histone chaperone TAF-I/SET/INHAT is required for transcription in vitro of chromatin templates.

PubMed

Gamble, Matthew J; Erdjument-Bromage, Hediye; Tempst, Paul; Freedman, Leonard P; Fisher, Robert P

2005-01-01

To uncover factors required for transcription by RNA polymerase II on chromatin, we fractionated a mammalian cell nuclear extract. We identified the histone chaperone TAF-I (also known as INHAT [inhibitor of histone acetyltransferase]), which was previously proposed to repress transcription, as a potent activator of chromatin transcription responsive to the vitamin D3 receptor or to Gal4-VP16. TAF-I associates with chromatin in vitro and can substitute for the related protein NAP-1 in assembling chromatin onto cloned DNA templates in cooperation with the remodeling enzyme ATP-dependent chromatin assembly factor (ACF). The chromatin assembly and transcriptional activation functions are distinct, however, and can be dissociated temporally. Efficient transcription of chromatin assembled with TAF-I still requires the presence of TAF-I during the polymerization reaction. Conversely, TAF-I cannot stimulate transcript elongation when added after the other factors necessary for assembly of a preinitiation complex on naked DNA. Thus, TAF-I is required to facilitate transcription at a step after chromatin assembly but before transcript elongation.

Suppression of HTLV-1 replication by Tax-mediated rerouting of the p13 viral protein to nuclear speckles

PubMed Central

Andresen, Vibeke; Pise-Masison, Cynthia A.; Sinha-Datta, Uma; Bellon, Marcia; Valeri, Valerio; Washington Parks, Robyn; Cecchinato, Valentina; Fukumoto, Risaku; Nicot, Christophe

2011-01-01

Disease development in human T-cell leukemia virus type 1 (HTLV-1)–infected individuals is positively correlated with the level of integrated viral DNA in T cells. HTLV-1 replication is positively regulated by Tax and Rex and negatively regulated by the p30 and HBZ proteins. In the present study, we demonstrate that HTLV-1 encodes another negative regulator of virus expression, the p13 protein. Expressed separately, p13 localizes to the mitochondria, whereas in the presence of Tax, part of it is ubiquitinated, stabilized, and rerouted to the nuclear speckles. The p13 protein directly binds Tax, decreases Tax binding to the CBP/p300 transcriptional coactivator, and, by reducing Tax transcriptional activity, suppresses viral expression. Because Tax stabilizes its own repressor, these findings suggest that HTLV-1 has evolved a complex mechanism to control its own replication. Further, these results highlight the importance of studying the function of the HTLV-1 viral proteins, not only in isolation, but also in the context of full viral replication. PMID:21677314

27 CFR 53.179 - Supporting evidence required in case of manufacturers tax involving exportations, uses, sales, or...

Code of Federal Regulations, 2012 CFR

2012-04-01

... chain of sales from the person who paid the tax to the ultimate purchaser, the evidence required to be... vendor retains such proof for 3 years from the date of the statement and will, upon request, supply such...

27 CFR 53.179 - Supporting evidence required in case of manufacturers tax involving exportations, uses, sales, or...

Code of Federal Regulations, 2013 CFR

2013-04-01

... chain of sales from the person who paid the tax to the ultimate purchaser, the evidence required to be... vendor retains such proof for 3 years from the date of the statement and will, upon request, supply such...

27 CFR 53.179 - Supporting evidence required in case of manufacturers tax involving exportations, uses, sales, or...

Code of Federal Regulations, 2010 CFR

2010-04-01

... chain of sales from the person who paid the tax to the ultimate purchaser, the evidence required to be... vendor retains such proof for 3 years from the date of the statement and will, upon request, supply such...

27 CFR 53.179 - Supporting evidence required in case of manufacturers tax involving exportations, uses, sales, or...

Code of Federal Regulations, 2011 CFR

2011-04-01

... chain of sales from the person who paid the tax to the ultimate purchaser, the evidence required to be... vendor retains such proof for 3 years from the date of the statement and will, upon request, supply such...

The tax oncoprotein of human T-cell leukemia virus type 1 associates with and persistently activates IkappaB kinases containing IKKalpha and IKKbeta.

PubMed

Chu, Z L; DiDonato, J A; Hawiger, J; Ballard, D W

1998-06-26

The Tax oncoprotein of human T-cell leukemia virus type 1 (HTLV1) chronically activates transcription factor NF-kappaB by a mechanism involving degradation of IkappaBalpha, an NF-kappaB-associated cytoplasmic inhibitor. Tax-induced breakdown of IkappaBalpha requires phosphorylation of the inhibitor at Ser-32 and Ser-36, which is also a prerequisite for the transient activation of NF-kappaB in cytokine-treated T lymphocytes. However, it remained unclear how Tax interfaces with the cellular NF-kappaB/IkappaB signaling machinery to generate a chronic rather than a transient NF-kappaB response. We now demonstrate that Tax associates with cytokine-inducible IkappaB kinase (IKK) complexes containing catalytic subunits IKKalpha and IKKbeta, which mediate phosphorylation of IkappaBalpha at Ser-32 and Ser-36. Unlike their transiently activated counterparts in cytokine-treated cells, Tax-associated forms of IKK are constitutively active in either Tax transfectants or HTLV1-infected T lymphocytes. Moreover, point mutations in Tax that ablate its IKK-binding function also prevent Tax-mediated activation of IKK and NF-kappaB. Together, these findings suggest that the persistent activation of NF-kappaB in HTLV1-infected T-cells is mediated by a direct Tax/IKK coupling mechanism.

Tax Compliance Inventory: TAX-I Voluntary tax compliance, enforced tax compliance, tax avoidance, and tax evasion

PubMed Central

Kirchler, Erich; Wahl, Ingrid

2010-01-01

Surveys on tax compliance and non-compliance often rely on ad hoc formulated items which lack standardization and empirical validation. We present an inventory to assess tax compliance and distinguish between different forms of compliance and non-compliance: voluntary versus enforced compliance, tax avoidance, and tax evasion. First, items to measure voluntary and enforced compliance, avoidance, and evasion were drawn up (collected from past research and newly developed), and tested empirically with the aim of producing four validated scales with a clear factorial structure. Second, findings from the first analyses were replicated and extended to validation on the basis of motivational postures. A standardized inventory is provided which can be used in surveys in order to collect data which are comparable across research focusing on self-reports. The inventory can be used in either of two ways: either in its entirety, or by applying the single scales independently, allowing an economical and fast assessment of different facets of tax compliance. PMID:20502612

Tax Compliance Inventory: TAX-I Voluntary tax compliance, enforced tax compliance, tax avoidance, and tax evasion.

PubMed

Kirchler, Erich; Wahl, Ingrid

2010-06-01

Surveys on tax compliance and non-compliance often rely on ad hoc formulated items which lack standardization and empirical validation. We present an inventory to assess tax compliance and distinguish between different forms of compliance and non-compliance: voluntary versus enforced compliance, tax avoidance, and tax evasion. First, items to measure voluntary and enforced compliance, avoidance, and evasion were drawn up (collected from past research and newly developed), and tested empirically with the aim of producing four validated scales with a clear factorial structure. Second, findings from the first analyses were replicated and extended to validation on the basis of motivational postures. A standardized inventory is provided which can be used in surveys in order to collect data which are comparable across research focusing on self-reports. The inventory can be used in either of two ways: either in its entirety, or by applying the single scales independently, allowing an economical and fast assessment of different facets of tax compliance.

26 CFR 301.6011-7 - Specified tax return preparers required to file individual income tax returns using magnetic media.

Code of Federal Regulations, 2011 CFR

2011-04-01

... individual income tax returns using magnetic media. 301.6011-7 Section 301.6011-7 Internal Revenue INTERNAL... to file individual income tax returns using magnetic media. (a) Definitions. (1) Magnetic media. For purposes of this section, the term magnetic media has the same meaning as in § 301.6011-2(a)(1). (2...

26 CFR 301.6011-7 - Specified tax return preparers required to file individual income tax returns using magnetic media.

Code of Federal Regulations, 2012 CFR

2012-04-01

... individual income tax returns using magnetic media. 301.6011-7 Section 301.6011-7 Internal Revenue INTERNAL... to file individual income tax returns using magnetic media. (a) Definitions. (1) Magnetic media. For purposes of this section, the term magnetic media has the same meaning as in § 301.6011-2(a)(1). (2...

26 CFR 301.6011-7 - Specified tax return preparers required to file individual income tax returns using magnetic media.

Code of Federal Regulations, 2013 CFR

2013-04-01

... individual income tax returns using magnetic media. 301.6011-7 Section 301.6011-7 Internal Revenue INTERNAL... to file individual income tax returns using magnetic media. (a) Definitions. (1) Magnetic media. For purposes of this section, the term magnetic media has the same meaning as in § 301.6011-2(a)(1). (2...

Tax Changes, Retirement, and Pensions.

ERIC Educational Resources Information Center

Sumberg, Alfred D.

1989-01-01

The 1986 amendments to the Age Discrimination in Employment Act and tax reforms from that year will require changes in retirement policies in higher education, especially pension plans, because of the extension of nondiscrimination rules to all tax-deferred annuities. (Author/MSE)

26 CFR 26.2662-1 - Generation-skipping transfer tax return requirements.

Code of Federal Regulations, 2010 CFR

2010-04-01

... transferor for which a gift tax return is not filed; or (ii) The inclusion ratio with respect to the trust, determined by reference to the transferor's gift tax return, is erroneous, the actual inclusion ratio being greater than the reported inclusion ratio. (iii) This paragraph (c)(3) does not apply if the trustee has...

The Law of Tax-Exempt Organizations. Third Edition.

ERIC Educational Resources Information Center

Hopkins, Bruce R.

This single-volume reference describes in detail the federal tax laws governing income tax exemption for qualified organizations. All categories of tax-exempt organizations are treated, as well as many related subjects, providing the conditions and requirements for protecting a tax-exempt status. Organized according to the subject's major…

48 CFR 29.305 - State and local tax exemptions.

Code of Federal Regulations, 2010 CFR

2010-10-01

... 48 Federal Acquisition Regulations System 1 2010-10-01 2010-10-01 false State and local tax... GENERAL CONTRACTING REQUIREMENTS TAXES State and Local Taxes 29.305 State and local tax exemptions. (a) Evidence of exemption. Evidence needed to establish exemption from State or local taxes depends on the...

IL-15 Deficient Tax Mice Reveal a Role for IL-1α in Tumor Immunity

PubMed Central

Rauch, Daniel A.; Harding, John C.; Ratner, Lee

2014-01-01

IL-15 is recognized as a promising candidate for tumor immunotherapy and has been described as both a promoter of cancer and a promoter of anti-cancer immunity. IL-15 was discovered in cells transformed by HTLV-1, the etiologic agent of adult T cell leukemia/lymphoma (ATL) and the human retrovirus that carries the Tax oncogene. We have developed the TAX-LUC mouse model of ATL in which Tax expression drives both malignant transformation and luciferase expression, enabling non-invasive imaging of tumorigenesis in real time. To identify the role of IL-15 in spontaneous development of lymphoma in vivo, an IL-15−/− TAX-LUC strain was developed and examined. The absence of IL-15 resulted in aggressive tumor growth and accelerated mortality and demonstrated that IL-15 was not required for Tax-mediated lymphoma but was essential for anti-tumor immunity. Further analysis revealed a unique transcriptional profile in tumor cells that arise in the absence of IL-15 that included a significant increase in the expression of IL-1α and IL-1α-regulated cytokines. Moreover, anti-IL-1α antibodies and an IL-1 receptor antagonist (Anakinra) were used to interrogate the potential of IL-1α targeted therapies in this model. Taken together, these findings identify IL-15 and IL-1α as therapeutic targets in lymphoma. PMID:24416335

78 FR 71468 - Rules Relating to Additional Medicare Tax

Federal Register 2010, 2011, 2012, 2013, 2014

2013-11-29

... Rules Relating to Additional Medicare Tax AGENCY: Internal Revenue Service (IRS), Treasury. ACTION... Insurance Tax on income above threshold amounts (``Additional Medicare Tax''), as added by the Affordable... to the implementation of Additional Medicare Tax, including the requirement to withhold Additional...

HTLV-1 Tax protein cooperates with Ras in protecting cells from apoptosis.

PubMed

Vajente, Nicola; Trevisan, Roberta; Saggioro, Daniela

2009-02-01

Tax protein of the human T-cell leukemia virus type 1 (HTLV-1) plays a critical role in HTLV-I-correlated diseases through its ability to deregulate the expression of a vast array of cellular genes. We have previously shown that Tax counteracts apoptosis induced by stimuli triggering mitochondria apoptotic pathway, most likely by activating CREB-mediated transcription and affecting the phosphorylation levels of CREB at Ser-133. Here, we report data that indicate the oncoprotein Ras as a possible mediator of Tax-induced apoptosis protection and suggest a possible role of Tax in Ras activation. In addition, using inhibitors of down stream effectors of Ras, we found that ERK signaling is the most relevant for Tax-mediated apoptosis protection. As a whole, our findings provide intriguing evidence of a possible link between Ras signaling and Tax capability to counteract apoptosis and to enhance P-CREB levels, and implicates a potential role for Ras in HTLV-1-induced diseases.

Sequences required for transcription termination at the intrinsic lambdatI terminator.

PubMed

Martínez-Trujillo, Miguel; Sánchez-Trujillo, Alejandra; Ceja, Víctor; Avila-Moreno, Federico; Bermúdez-Cruz, Rosa María; Court, Donald; Montañez, Cecilia

2010-02-01

The lambdatI terminator is located approximately 280 bp beyond the lambdaint gene, and it has a typical structure of an intrinsic terminator. To identify sequences required for lambdatI transcription termination a set of deletion mutants were generated, either from the 5' or the 3' end onto the lambdatI region. The termination efficiency was determined by measuring galactokinase (galK) levels by Northern blot assays and by in vitro transcription termination. The importance of the uridines and the stability of the stem structure in the termination were demonstrated. The nontranscribed DNA beyond the 3' end also affects termination. Additionally, sequences upstream have a small effect on transcription termination. The in vivo RNA termination sites at lambdatI were determined by S1 mapping and were located at 8 different positions. Processing of transcripts from the 3' end confirmed the importance of the hairpin stem in protection against exonuclease.

An RNA Interference Screen Identifies the Deubiquitinase STAMBPL1 as a Critical Regulator of Human T-Cell Leukemia Virus Type 1 Tax Nuclear Export and NF-κB Activation

PubMed Central

Lavorgna, Alfonso

2012-01-01

The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein actively shuttles between the nucleus, where it interacts with transcriptional and splicing regulatory proteins, and the cytoplasm, where it activates NF-κB. Posttranslational modifications of Tax such as ubiquitination regulate its subcellular localization and hence its function; however, the regulation of Tax trafficking and NF-κB activation by host factors is poorly understood. By screening a deubiquitinating (DUB) enzyme small interfering RNA (siRNA) library, we identified the metalloprotease STAM-binding protein-like 1 (STAMBPL1) as a positive regulator of Tax-mediated NF-κB activation. Overexpression of wild-type STAMBPL1, but not a catalytically inactive mutant, enhanced Tax-mediated NF-κB activation, whereas silencing of STAMBPL1 with siRNA impaired Tax activation of both the canonical and noncanonical NF-κB signaling pathways. STAMBPL1 regulated Tax-induced NF-κB signaling indirectly by controlling Tax nuclear/cytoplasmic transport and was required for DNA damage-induced Tax nuclear export. Together, these results reveal that the deubiquitinase STAMBPL1 is a key regulator of Tax trafficking and function. PMID:22258247

Price and Tax Measures and Illicit Trade in the Framework Convention on Tobacco Control: What We Know and What Research Is Required

PubMed Central

2013-01-01

Introduction: Article 6 of the Framework Convention on Tobacco Control commits Parties to use tax and price policies to reduce tobacco use, whereas Article 15 commits Parties to implement measures to eliminate the illicit trade in tobacco products. This paper identifies research gaps/needs, especially in low- and middle-income countries, which, if adequately addressed, would help in implementing Articles 6 and 15. Methods: Based on a recent comprehensive review on the impact of tax and price on tobacco consumption and a summary of reviews and narratives about the illicit tobacco market, research gaps are identified. Results: Countries have highly diverse research needs, depending on the stage of the tobacco epidemic, previous research and data availability, and making a ranking of research needs infeasible. Broad issues for further research are the following: (1) monitoring tobacco consumption, prices, and taxes, (2) assessing the effectiveness of the tax structure in generating revenue and reducing tobacco use, (3) strengthening the tax administration system in order to reduce tax evasion and tax avoidance, (4) improving our understanding of the political economy of tobacco tax policy, and (5) employing a multidisciplinary approach to assessing the magnitude of illicit tobacco trade. Conclusions: At a technical level, the case for increasing excise taxes to improve public health and increase government revenue is easily made, but the political and policy environment is often not supportive. In order to effectively impact policy, the required approach would typically make use of rigorous economic techniques, and be cognizant of the political economy of raising excise taxes. PMID:22987785

Price and tax measures and illicit trade in the framework convention on tobacco control: what we know and what research is required.

PubMed

van Walbeek, Corne; Blecher, Evan; Gilmore, Anna; Ross, Hana

2013-04-01

Article 6 of the Framework Convention on Tobacco Control commits Parties to use tax and price policies to reduce tobacco use, whereas Article 15 commits Parties to implement measures to eliminate the illicit trade in tobacco products. This paper identifies research gaps/needs, especially in low- and middle-income countries, which, if adequately addressed, would help in implementing Articles 6 and 15. Based on a recent comprehensive review on the impact of tax and price on tobacco consumption and a summary of reviews and narratives about the illicit tobacco market, research gaps are identified. Countries have highly diverse research needs, depending on the stage of the tobacco epidemic, previous research and data availability, and making a ranking of research needs infeasible. Broad issues for further research are the following: (1) monitoring tobacco consumption, prices, and taxes, (2) assessing the effectiveness of the tax structure in generating revenue and reducing tobacco use, (3) strengthening the tax administration system in order to reduce tax evasion and tax avoidance, (4) improving our understanding of the political economy of tobacco tax policy, and (5) employing a multidisciplinary approach to assessing the magnitude of illicit tobacco trade. At a technical level, the case for increasing excise taxes to improve public health and increase government revenue is easily made, but the political and policy environment is often not supportive. In order to effectively impact policy, the required approach would typically make use of rigorous economic techniques, and be cognizant of the political economy of raising excise taxes.

Induction of HoxB Transcription by Retinoic Acid Requires Actin Polymerization

PubMed Central

Ferrai, Carmelo; Naum-Onganía, Gabriela; Longobardi, Elena; Palazzolo, Martina; Disanza, Andrea; Diaz, Victor M.; Crippa, Massimo P.; Scita, Giorgio

2009-01-01

We have analyzed the role of actin polymerization in retinoic acid (RA)-induced HoxB transcription, which is mediated by the HoxB regulator Prep1. RA induction of the HoxB genes can be prevented by the inhibition of actin polymerization. Importantly, inhibition of actin polymerization specifically affects the transcription of inducible Hox genes, but not that of their transcriptional regulators, the RARs, nor of constitutively expressed, nor of actively transcribed Hox genes. RA treatment induces the recruitment to the HoxB2 gene enhancer of a complex composed of “elongating” RNAPII, Prep1, β-actin, and N-WASP as well as the accessory splicing components p54Nrb and PSF. We show that inhibition of actin polymerization prevents such recruitment. We conclude that inducible Hox genes are selectively sensitive to the inhibition of actin polymerization and that actin polymerization is required for the assembly of a transcription complex on the regulatory region of the Hox genes. PMID:19477923

Induction of HoxB transcription by retinoic acid requires actin polymerization.

PubMed

Ferrai, Carmelo; Naum-Onganía, Gabriela; Longobardi, Elena; Palazzolo, Martina; Disanza, Andrea; Diaz, Victor M; Crippa, Massimo P; Scita, Giorgio; Blasi, Francesco

2009-08-01

We have analyzed the role of actin polymerization in retinoic acid (RA)-induced HoxB transcription, which is mediated by the HoxB regulator Prep1. RA induction of the HoxB genes can be prevented by the inhibition of actin polymerization. Importantly, inhibition of actin polymerization specifically affects the transcription of inducible Hox genes, but not that of their transcriptional regulators, the RARs, nor of constitutively expressed, nor of actively transcribed Hox genes. RA treatment induces the recruitment to the HoxB2 gene enhancer of a complex composed of "elongating" RNAPII, Prep1, beta-actin, and N-WASP as well as the accessory splicing components p54Nrb and PSF. We show that inhibition of actin polymerization prevents such recruitment. We conclude that inducible Hox genes are selectively sensitive to the inhibition of actin polymerization and that actin polymerization is required for the assembly of a transcription complex on the regulatory region of the Hox genes.

Two Waves of Transcription Are Required for Long-Term Memory in the Honeybee

ERIC Educational Resources Information Center

Lefer, Damien; Perisse, Emmanuel; Hourcade, Benoit; Sandoz, JeanChristophe; Devaud, Jean-Marc

2013-01-01

Storage of information into long-term memory (LTM) usually requires at least two waves of transcription in many species. However, there is no clear evidence of this phenomenon in insects, which are influential models for memory studies. We measured retention in honeybees after injecting a transcription inhibitor at different times before and after…

27 CFR 19.226 - Gauges for tax determination.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 27 Alcohol, Tobacco Products and Firearms 1 2011-04-01 2011-04-01 false Gauges for tax determination. 19.226 Section 19.226 Alcohol, Tobacco Products and Firearms ALCOHOL AND TOBACCO TAX AND TRADE BUREAU, DEPARTMENT OF THE TREASURY LIQUORS DISTILLED SPIRITS PLANTS Distilled Spirits Taxes Requirements...

47 CFR 32.7200 - Operating taxes.

Code of Federal Regulations, 2010 CFR

2010-10-01

... FOR TELECOMMUNICATIONS COMPANIES Instructions For Other Income Accounts § 32.7200 Operating taxes. Class B telephone companies shall use this account for operating taxes of the type and character required of Class A companies in Accounts 7210 through 7250. [67 FR 5698, Feb. 6, 2002] ...

27 CFR 19.227 - Determination of the tax.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 27 Alcohol, Tobacco Products and Firearms 1 2011-04-01 2011-04-01 false Determination of the tax. 19.227 Section 19.227 Alcohol, Tobacco Products and Firearms ALCOHOL AND TOBACCO TAX AND TRADE BUREAU, DEPARTMENT OF THE TREASURY LIQUORS DISTILLED SPIRITS PLANTS Distilled Spirits Taxes Requirements for Gauging...

An Alternative Splice Product of IκB Kinase (IKKγ), IKKγ-Δ, Differentially Mediates Cytokine and Human T-Cell Leukemia Virus Type 1 Tax-Induced NF-κB Activation

PubMed Central

Hai, Tao; Yeung, Man-Lung; Wood, Thomas G.; Wei, Yuanfen; Yamaoka, Shoji; Gatalica, Zoran; Jeang, Kuan-Teh; Brasier, Allan R.

2006-01-01

NF-κB is an inducible transcription factor mediating innate immune responses whose activity is controlled by the multiprotein IκB kinase (IKK) “signalsome”. The core IKK consists of two catalytic serine kinases, IKKα and IKKβ, and a noncatalytic subunit, IKKγ. IKKγ is required for IKK activity by mediating kinase oligomerization and serving to couple the core catalytic subunits to upstream mitogen-activated protein 3-kinase cascades. We have discovered an alternatively spliced IKKγ mRNA isoform, encoding an in-frame deletion of exon 5, termed IKKγ-Δ. Using a specific reverse transcription-PCR assay, we find that IKKγ-Δ is widely expressed in cultured human cells and normal human tissues. Because IKKγ-Δ protein is lacking a critical coiled-coil domain important in protein-protein interactions, we sought to determine its signaling properties by examining its ability to self associate, couple to activators of the canonical pathway, and mediate human T-cell leukemia virus type 1 (HTLV-1) Tax-induced NF-κB activity. Coimmunoprecipitation and confocal colocalization assays indicate IKKγ-Δ has strong homo- and heterotypic association with wild-type (WT) IKKγ and, like IKKγ WT, associates with the IKKβ kinase. Similarly, IKKγ-Δ mediates IKK kinase activity and downstream NF-κB-dependent transcription in response to tumor necrosis factor (TNF) and the NF-κB-inducing kinase-IKKα signaling pathway. Surprisingly, however, in contrast to IKKγ WT, IKKγ-Δ is not able to mediate HTLV-1 Tax-induced NF-κB-dependent transcription, even though IKKγ-Δ binds and colocalizes with Tax. These observations suggest that IKKγ-Δ is a functionally distinct alternatively spliced mRNA product differentially mediating TNF-induced, but not Tax-induced, signals converging on the IKK signalsome. Differing levels of IKKγ-Δ expression, therefore, may affect signal transduction cascades coupling to IKK. PMID:16611882

75 FR 46844 - Excise Taxes on Prohibited Tax Shelter Transactions and Related Disclosure Requirements...

Federal Register 2010, 2011, 2012, 2013, 2014

2010-08-04

... continues to read in part as follows: Authority: 26 U.S.C. 7805 * * * 0 Par. 2. Section 53.4965-2 is amended... * * * 0 Par. 7. Section 54.6011-1 is amended by revising paragraph (c)(2) to read as follows: Sec. 54.6011... shelter transactions to which tax-exempt entities are parties; sections 6033(a)(2) and 6011(g), relating...

27 CFR 25.166 - Payment of reduced rate of tax.

Code of Federal Regulations, 2010 CFR

2010-04-01

... BUREAU, DEPARTMENT OF THE TREASURY LIQUORS BEER Tax on Beer Preparation and Remittance of Tax Returns... the reduced rate of tax on beer may, upon filing the notice required by § 25.167, pay the reduced rate of tax on beer by return for deferred payment of tax as provided in § 25.164 or by prepayment return...

27 CFR 25.166 - Payment of reduced rate of tax.

Code of Federal Regulations, 2012 CFR

2012-04-01

... BUREAU, DEPARTMENT OF THE TREASURY LIQUORS BEER Tax on Beer Preparation and Remittance of Tax Returns... the reduced rate of tax on beer may, upon filing the notice required by § 25.167, pay the reduced rate of tax on beer by return for deferred payment of tax as provided in § 25.164 or by prepayment return...

27 CFR 25.166 - Payment of reduced rate of tax.

Code of Federal Regulations, 2013 CFR

2013-04-01

... BUREAU, DEPARTMENT OF THE TREASURY ALCOHOL BEER Tax on Beer Preparation and Remittance of Tax Returns... the reduced rate of tax on beer may, upon filing the notice required by § 25.167, pay the reduced rate of tax on beer by return for deferred payment of tax as provided in § 25.164 or by prepayment return...

27 CFR 25.166 - Payment of reduced rate of tax.

Code of Federal Regulations, 2014 CFR

2014-04-01

... BUREAU, DEPARTMENT OF THE TREASURY ALCOHOL BEER Tax on Beer Preparation and Remittance of Tax Returns... the reduced rate of tax on beer may, upon filing the notice required by § 25.167, pay the reduced rate of tax on beer by return for deferred payment of tax as provided in § 25.164 or by prepayment return...

27 CFR 25.166 - Payment of reduced rate of tax.

Code of Federal Regulations, 2011 CFR

2011-04-01

... BUREAU, DEPARTMENT OF THE TREASURY LIQUORS BEER Tax on Beer Preparation and Remittance of Tax Returns... the reduced rate of tax on beer may, upon filing the notice required by § 25.167, pay the reduced rate of tax on beer by return for deferred payment of tax as provided in § 25.164 or by prepayment return...

76 FR 42038 - Determining the Amount of Taxes Paid for Purposes of the Foreign Tax Credit

Federal Register 2010, 2011, 2012, 2013, 2014

2011-07-18

... investment condition''). The direct investment condition requires that the U.S. party's share of the foreign...) of this section if the foreign payment were an amount of tax paid. (3) Direct investment. The U.S... claim direct and indirect foreign tax credits. DATES: Effective Date: These regulations are effective on...

27 CFR 53.182 - Supporting evidence required in case of tax-paid articles used for further manufacture.

Code of Federal Regulations, 2010 CFR

2010-04-01

... required in case of tax-paid articles used for further manufacture. 53.182 Section 53.182 Alcohol, Tobacco... articles used for further manufacture. (a) Evidence to be submitted by claimant. No claim for credit or... material in the manufacture or production of, or as a component part of, a second article manufactured or...

27 CFR 27.77 - Standard effective tax rate.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 27 Alcohol, Tobacco Products and Firearms 1 2011-04-01 2011-04-01 false Standard effective tax rate. 27.77 Section 27.77 Alcohol, Tobacco Products and Firearms ALCOHOL AND TOBACCO TAX AND TRADE... Requirements Wine and Flavors Content of Distilled Spirits § 27.77 Standard effective tax rate. (a) In lieu of...

The Human T-Lymphotropic Virus Type 1 Tax Protein Inhibits Nonsense-Mediated mRNA Decay by Interacting with INT6/EIF3E and UPF1

PubMed Central

Mocquet, Vincent; Neusiedler, Julia; Rende, Francesca; Cluet, David; Robin, Jean-Philippe; Terme, Jean-Michel; Duc Dodon, Madeleine; Wittmann, Jürgen; Morris, Christelle; Le Hir, Hervé; Ciminale, Vincenzo

2012-01-01

In this report, we analyzed whether the degradation of mRNAs by the nonsense-mediated mRNA decay (NMD) pathway was affected in human T-lymphotropic virus type 1 (HTLV-1)-infected cells. This pathway was indeed strongly inhibited in C91PL, HUT102, and MT2 cells, and such an effect was also observed by the sole expression of the Tax protein in Jurkat and HeLa cells. In line with this activity, Tax binds INT6/EIF3E (here called INT6), which is a subunit of the translation initiation factor eukaryotic initiation factor 3 (eIF3) required for efficient NMD, as well as the NMD core factor upstream frameshift protein 1 (UPF1). It was also observed that Tax expression alters the morphology of processing bodies (P-bodies), the cytoplasmic structures which concentrate RNA degradation factors. The presence of UPF1 in these subcellular compartments was increased by Tax, whereas that of INT6 was decreased. In line with these effects, the level of the phosphorylated form of UPF1 was increased in the presence of Tax. Analysis of several mutants of the viral protein showed that the interaction with INT6 is necessary for NMD inhibition. The alteration of mRNA stability was observed to affect viral transcripts, such as that coding for the HTLV-1 basic leucine zipper factor (HBZ), and also several cellular mRNAs sensitive to the NMD pathway. Our data indicate that the effect of Tax on viral and cellular gene expression is not restricted to transcriptional control but can also involve posttranscriptional regulation. PMID:22553336

Tax Incentives for Education. Hearing before the Committee on Finance. United States Senate, One Hundredth Congress, Second Session.

ERIC Educational Resources Information Center

Congress of the U.S., Washington, DC. Senate Committee on Finance.

The transcript of a hearing before the Senate Committee on Finance concerning tax incentives for education is presented. The statements of committee members and public witnesses testimony, both oral and written, are provided, as well as letters of support. Current tax expenditures for financial aid to college students, including student loan…

78 FR 59313 - Requirement of a Section 4959 Excise Tax Return and Time for Filing the Return; Correction

Federal Register 2010, 2011, 2012, 2013, 2014

2013-09-26

... liable for the excise tax for failure to meet the community health needs assessment requirements for any... Revenue Code. Need for Correction As published, the notice of proposed rulemaking (REG-115300-13) contains errors that are misleading and are in need of clarification. Correction to Publication Accordingly...

78 FR 59228 - Requirement of a Section 4959 Excise Tax Return and Time for Filing the Return; Correction

Federal Register 2010, 2011, 2012, 2013, 2014

2013-09-26

... the community health needs assessment (CHNA) requirements for any taxable year. DATES: This correction... the reporting of the excise tax under section 4959 of the Internal Revenue Code. Need for Correction... misleading and are in need of clarification. Correction of Publication Accordingly, the final and temporary...

2 CFR 200.470 - Taxes (including Value Added Tax).

Code of Federal Regulations, 2014 CFR

2014-01-01

... 2 Grants and Agreements 1 2014-01-01 2014-01-01 false Taxes (including Value Added Tax). 200.470... Cost § 200.470 Taxes (including Value Added Tax). (a) For states, local governments and Indian tribes... Federal government for the taxes, interest, and penalties. (c) Value Added Tax (VAT) Foreign taxes charged...

I-mfa domain proteins specifically interact with HTLV-1 Tax and repress its transactivating functions.

PubMed

Kusano, Shuichi; Yoshimitsu, Makoto; Hachiman, Miho; Ikeda, Masanori

2015-12-01

The I-mfa domain proteins HIC (also known as MDFIC) and I-mfa (also known as MDFI) are candidate tumor suppressor genes that are involved in cellular and viral transcriptional regulation. Here, we show that HIC and I-mfa directly interact with human T-cell leukemia virus type-1 (HTLV-1) Tax protein in vitro. In addition, HIC and I-mfa repress Tax-dependent transactivation of an HTLV-1 long terminal repeat (LTR) reporter construct in COS-1, Jurkat and high-Tax-producing HTLV-1-infected T cells. HIC also interacts with Tax through its I-mfa domain in vivo and represses Tax-dependent transactivation of HTLV-1 LTR and NF-κB reporter constructs in an interaction-dependent manner. Furthermore, we show that HIC decreases the nuclear distribution and stimulates the proteasomal degradation of Tax. These data reveal that HIC specifically interacts with HTLV-1 Tax and negatively regulates Tax transactivational activity by altering its subcellular distribution and stability. Copyright © 2015 Elsevier Inc. All rights reserved.

Unusually long-lived pause required for regulation of a Rho-dependent transcription terminator.

PubMed

Hollands, Kerry; Sevostiyanova, Anastasia; Groisman, Eduardo A

2014-05-13

Up to half of all transcription termination events in bacteria rely on the RNA-dependent helicase Rho. However, the nucleic acid sequences that promote Rho-dependent termination remain poorly characterized. Defining the molecular determinants that confer Rho-dependent termination is especially important for understanding how such terminators can be regulated in response to specific signals. Here, we identify an extraordinarily long-lived pause at the site where Rho terminates transcription in the 5'-leader region of the Mg(2+) transporter gene mgtA in Salmonella enterica. We dissect the sequence elements required for prolonged pausing in the mgtA leader and establish that the remarkable longevity of this pause is required for a riboswitch to stimulate Rho-dependent termination in the mgtA leader region in response to Mg(2+) availability. Unlike Rho-dependent terminators described previously, where termination occurs at multiple pause sites, there is a single site of transcription termination directed by Rho in the mgtA leader. Our data suggest that Rho-dependent termination events that are subject to regulation may require elements distinct from those operating at constitutive Rho-dependent terminators.

Unusually long-lived pause required for regulation of a Rho-dependent transcription terminator

PubMed Central

Hollands, Kerry; Sevostiyanova, Anastasia; Groisman, Eduardo A.

2014-01-01

Up to half of all transcription termination events in bacteria rely on the RNA-dependent helicase Rho. However, the nucleic acid sequences that promote Rho-dependent termination remain poorly characterized. Defining the molecular determinants that confer Rho-dependent termination is especially important for understanding how such terminators can be regulated in response to specific signals. Here, we identify an extraordinarily long-lived pause at the site where Rho terminates transcription in the 5′-leader region of the Mg2+ transporter gene mgtA in Salmonella enterica. We dissect the sequence elements required for prolonged pausing in the mgtA leader and establish that the remarkable longevity of this pause is required for a riboswitch to stimulate Rho-dependent termination in the mgtA leader region in response to Mg2+ availability. Unlike Rho-dependent terminators described previously, where termination occurs at multiple pause sites, there is a single site of transcription termination directed by Rho in the mgtA leader. Our data suggest that Rho-dependent termination events that are subject to regulation may require elements distinct from those operating at constitutive Rho-dependent terminators. PMID:24778260

26 CFR 301.6019-1 - Gift tax returns.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 18 2010-04-01 2010-04-01 false Gift tax returns. 301.6019-1 Section 301.6019-1... ADMINISTRATION PROCEDURE AND ADMINISTRATION Information and Returns Returns and Records § 301.6019-1 Gift tax returns. For provisions relating to requirement of gift tax returns, see §§ 25.6019-1 to 25.6019-4...

Integrating ICT Skills and Tax Software in Tax Education: A Survey of Malaysian Tax Practitioners' Perspectives

ERIC Educational Resources Information Center

Ling, Lai Ming; Nawawi, Nurul Hidayah Ahamad

2010-01-01

Purpose: This study aims to examine the ICT skills needed by a fresh accounting graduate when first joining a tax firm; to find out usage of electronic tax (e-tax) applications in tax practice; to assess the rating of senior tax practitioners on fresh graduates' ICT and e-tax applications skills; and to solicit tax practitioners' opinion regarding…

Distinguishing community benefits: tax exemption versus organizational legitimacy.

PubMed

Byrd, James D; Landry, Amy

2012-01-01

US policymakers continue to call into question the tax-exempt status of hospitals. As nonprofit tax-exempt entities, hospitals are required by the Internal Revenue Service (IRS) to report the type and cost of community benefits they provide. Institutional theory indicates that organizations derive organizational legitimacy from conforming to the expectations of their environment. Expectations from the state and federal regulators (the IRS, state and local taxing authorities in particular) and the community require hospitals to provide community benefits to achieve legitimacy. This article examines community benefit through an institutional theory framework, which includes regulative (laws and regulation), normative (certification and accreditation), and cultural-cognitive (relationship with the community including the provision of community benefits) pillars. Considering a review of the results of a 2006 IRS study of tax-exempt hospitals, the authors propose a model of hospital community benefit behaviors that distinguishes community benefits between cost-quantifiable activities appropriate for justifying tax exemption and unquantifiable activities that only contribute to hospitals' legitimacy.

I-mfa domain proteins specifically interact with HTLV-1 Tax and repress its transactivating functions

DOE Office of Scientific and Technical Information (OSTI.GOV)

Kusano, Shuichi, E-mail: skusano@m2.kufm.kagoshima-u.ac.jp; Yoshimitsu, Makoto; Hachiman, Miho

The I-mfa domain proteins HIC (also known as MDFIC) and I-mfa (also known as MDFI) are candidate tumor suppressor genes that are involved in cellular and viral transcriptional regulation. Here, we show that HIC and I-mfa directly interact with human T-cell leukemia virus type-1 (HTLV-1) Tax protein in vitro. In addition, HIC and I-mfa repress Tax-dependent transactivation of an HTLV-1 long terminal repeat (LTR) reporter construct in COS-1, Jurkat and high-Tax-producing HTLV-1-infected T cells. HIC also interacts with Tax through its I-mfa domain in vivo and represses Tax-dependent transactivation of HTLV-1 LTR and NF-κB reporter constructs in an interaction-dependent manner.more » Furthermore, we show that HIC decreases the nuclear distribution and stimulates the proteasomal degradation of Tax. These data reveal that HIC specifically interacts with HTLV-1 Tax and negatively regulates Tax transactivational activity by altering its subcellular distribution and stability. - Highlights: • I-mfa domain proteins, HIC and I-mfa, specifically interact with HTLV-1 Tax. • HIC and I-mfa repress the Tax-dependent transactivation of HTLV-1 LTR. • HIC represses the Tax-dependent transactivation of NF-κΒ. • HIC decreases the nuclear distribution of Tax. • HIC stimulates the proteasomal degradation of Tax.« less

26 CFR 301.6111-2 - Confidential corporate tax shelters.

Code of Federal Regulations, 2010 CFR

2010-04-01

... this section, registration shall in all events be required with respect to any interests in the... claimed to be proprietary or exclusive to the tax shelter promoter or any party other than the offeree. (2... any tax advisor (including a tax advisor independent from all other entities involved in the...

New tax law hobbles tax-exempt hospitals.

PubMed

Goldblatt, S J

1982-03-01

The Economic Recovery Tax Act of 1981 left tax-exempt hospitals at a significant disadvantage in the competition for capital. Although the new law's accelerated depreciation schedules and liberalized investment tax credits contain some marginal benefits for tax-exempt hospitals, these benefits are probably more than offset by the impact of the law on charitable giving.

Niclosamide, an anti-helminthic molecule, downregulates the retroviral oncoprotein Tax and pro-survival Bcl-2 proteins in HTLV-1-transformed T lymphocytes

PubMed Central

Chen, Li; Liu, Xin; Belani, Chandra; Cheng, Hua

2015-01-01

Adult T cell leukemia and lymphoma (ATL) is a highly aggressive form of hematological malignancy and is caused by chronic infection of human T cell leukemia virus type 1 (HTLV-1). The viral genome encodes an oncogenic protein, Tax, which plays a key role in transactivating viral gene transcription and in deregulating cellular oncogenic signaling to promote survival, proliferation and transformation of virally infected T cells. Hence, Tax is a desirable therapeutic target, particularly at early stage of HTLV-1-mediated oncogenesis. We here show that niclosamide, an anti-helminthic molecule, induced apoptosis of HTLV-1-transformed T cells. Niclosamide facilitated degradation of the Tax protein in proteasome. Consistent with niclosamide-mediated Tax degradation, this compound inhibited activities of MAPK/ERK1/2 and IκB kinases. In addition, niclosamide downregulated Stat3 and pro-survival Bcl-2 family members such as Mcl-1 and repressed the viral gene transcription of HTLV-1 through induction of Tax degradation. Since Tax, Stat3 and Mcl-1 are crucial molecules for promoting survival and growth of HTLV-1-transformed T cells, our findings demonstrate a novel mechanism of niclosamide in inducing Tax degradation and downregulating various cellular pro-survival molecules, thereby promoting apoptosis of HTLV-1-associated leukemia cells. PMID:26116531

Niclosamide, an anti-helminthic molecule, downregulates the retroviral oncoprotein Tax and pro-survival Bcl-2 proteins in HTLV-1-transformed T lymphocytes.

PubMed

Xiang, Di; Yuan, Yunsheng; Chen, Li; Liu, Xin; Belani, Chandra; Cheng, Hua

2015-08-14

Adult T cell leukemia and lymphoma (ATL) is a highly aggressive form of hematological malignancy and is caused by chronic infection of human T cell leukemia virus type 1 (HTLV-1). The viral genome encodes an oncogenic protein, Tax, which plays a key role in transactivating viral gene transcription and in deregulating cellular oncogenic signaling to promote survival, proliferation and transformation of virally infected T cells. Hence, Tax is a desirable therapeutic target, particularly at early stage of HTLV-1-mediated oncogenesis. We here show that niclosamide, an anti-helminthic molecule, induced apoptosis of HTLV-1-transformed T cells. Niclosamide facilitated degradation of the Tax protein in proteasome. Consistent with niclosamide-mediated Tax degradation, this compound inhibited activities of MAPK/ERK1/2 and IκB kinases. In addition, niclosamide downregulated Stat3 and pro-survival Bcl-2 family members such as Mcl-1 and repressed the viral gene transcription of HTLV-1 through induction of Tax degradation. Since Tax, Stat3 and Mcl-1 are crucial molecules for promoting survival and growth of HTLV-1-transformed T cells, our findings demonstrate a novel mechanism of niclosamide in inducing Tax degradation and downregulating various cellular pro-survival molecules, thereby promoting apoptosis of HTLV-1-associated leukemia cells. Copyright © 2015 Elsevier Inc. All rights reserved.

Profilin Is Required for Optimal Actin-Dependent Transcription of Respiratory Syncytial Virus Genome RNA

PubMed Central

Burke, Emily; Mahoney, Nicole M.; Almo, Steven C.; Barik, Sailen

2000-01-01

Transcription of human respiratory syncytial virus (RSV) genome RNA exhibited an obligatory need for the host cytoskeletal protein actin. Optimal transcription, however, required the participation of another cellular protein that was characterized as profilin by a number of criteria. The amino acid sequence of the protein, purified on the basis of its transcription-optimizing activity in vitro, exactly matched that of profilin. RSV transcription was inhibited 60 to 80% by antiprofilin antibody or poly-l-proline, molecules that specifically bind profilin. Native profilin, purified from extracts of lung epithelial cells by affinity binding to a poly-l-proline matrix, stimulated the actin-saturated RSV transcription by 2.5- to 3-fold. Recombinant profilin, expressed in bacteria, stimulated viral transcription as effectively as the native protein and was also inhibited by poly-l-proline. Profilin alone, in the absence of actin, did not activate viral transcription. It is estimated that at optimal levels of transcription, every molecule of viral genomic RNA associates with approximately the following number of protein molecules: 30 molecules of L, 120 molecules of phosphoprotein P, and 60 molecules each of actin and profilin. Together, these results demonstrated for the first time a cardinal role for profilin, an actin-modulatory protein, in the transcription of a paramyxovirus RNA genome. PMID:10623728

Human T-cell leukemia virus type 1 Tax and cell cycle progression: role of cyclin D-cdk and p110Rb.

PubMed

Neuveut, C; Low, K G; Maldarelli, F; Schmitt, I; Majone, F; Grassmann, R; Jeang, K T

1998-06-01

Human T-cell leukemia virus type 1 is etiologically linked to the development of adult T-cell leukemia and various human neuropathies. The Tax protein of human T-cell leukemia virus type I has been implicated in cellular transformation. Like other oncoproteins, such as Myc, Jun, and Fos, Tax is a transcriptional activator. How it mechanistically dysregulates the cell cycle is unclear. Previously, it was suggested that Tax affects cell-phase transition by forming a direct protein-protein complex with p16(INK4a), thereby inactivating an inhibitor of G1-to-S-phase progression. Here we show that, in T cells deleted for p16(INK4a), Tax can compel an egress of cells from G0/G1 into S despite the absence of serum. We also show that in undifferentiated myocytes, expression of Tax represses cellular differentiation. In both settings, Tax expression was found to increase cyclin D-cdk activity and to enhance pRb phosphorylation. In T cells, a Tax-associated increase in steady-state E2F2 protein was also documented. In searching for a molecular explanation for these observations, we found that Tax forms a protein-protein complex with cyclin D3, whereas a point-mutated and transcriptionally inert Tax mutant failed to form such a complex. Interestingly, expression of wild-type Tax protein in cells was also correlated with the induction of a novel hyperphosphorylated cyclin D3 protein. Taken together, these findings suggest that Tax might directly influence cyclin D-cdk activity and function, perhaps by a route independent of cdk inhibitors such as p16(INK4a).

Excise Tax Avoidance: The Case of State Cigarette Taxes

PubMed Central

DeCicca, Philip; Kenkel, Donald; Liu, Feng

2013-01-01

We conduct an applied welfare economics analysis of cigarette tax avoidance. We develop an extension of the standard formula for the optimal Pigouvian corrective tax to incorporate the possibility that consumers avoid the tax by making purchases in nearby lower-tax jurisdictions. To provide a key parameter for our formula, we estimate a structural endogenous switching regression model of border-crossing and cigarette prices. In illustrative calculations, we find that for many states, after taking into account tax avoidance the optimal tax is at least 20 percent smaller than the standard Pigouvian tax that simply internalizes external costs. Our empirical estimate that tax avoidance strongly responds to the price differential is the main reason for this result. We also use our results to examine the benefits of replacing avoidable state excise taxes with a harder-to-avoid federal excise tax on cigarettes. PMID:24140760

Excise tax avoidance: the case of state cigarette taxes.

PubMed

DeCicca, Philip; Kenkel, Donald; Liu, Feng

2013-12-01

We conduct an applied welfare economics analysis of cigarette tax avoidance. We develop an extension of the standard formula for the optimal Pigouvian corrective tax to incorporate the possibility that consumers avoid the tax by making purchases in nearby lower tax jurisdictions. To provide a key parameter for our formula, we estimate a structural endogenous switching regression model of border-crossing and cigarette prices. In illustrative calculations, we find that for many states, after taking into account tax avoidance the optimal tax is at least 20% smaller than the standard Pigouvian tax that simply internalizes external costs. Our empirical estimate that tax avoidance strongly responds to the price differential is the main reason for this result. We also use our results to examine the benefits of replacing avoidable state excise taxes with a harder-to-avoid federal excise tax on cigarettes. Copyright © 2013 Elsevier B.V. All rights reserved.

Implementation of meiosis prophase I programme requires a conserved retinoid-independent stabilizer of meiotic transcripts

PubMed Central

Abby, Emilie; Tourpin, Sophie; Ribeiro, Jonathan; Daniel, Katrin; Messiaen, Sébastien; Moison, Delphine; Guerquin, Justine; Gaillard, Jean-Charles; Armengaud, Jean; Langa, Francina; Toth, Attila; Martini, Emmanuelle; Livera, Gabriel

2016-01-01

Sexual reproduction is crucially dependent on meiosis, a conserved, specialized cell division programme that is essential for the production of haploid gametes. Here we demonstrate that fertility and the implementation of the meiotic programme require a previously uncharacterized meiosis-specific protein, MEIOC. Meioc invalidation in mice induces early and pleiotropic meiotic defects in males and females. MEIOC prevents meiotic transcript degradation and interacts with an RNA helicase that binds numerous meiotic mRNAs. Our results indicate that proper engagement into meiosis necessitates the specific stabilization of meiotic transcripts, a previously little-appreciated feature in mammals. Remarkably, the upregulation of MEIOC at the onset of meiosis does not require retinoic acid and STRA8 signalling. Thus, we propose that the complete induction of the meiotic programme requires both retinoic acid-dependent and -independent mechanisms. The latter process involving post-transcriptional regulation likely represents an ancestral mechanism, given that MEIOC homologues are conserved throughout multicellular animals. PMID:26742488

The Region between Amino Acids 245 and 265 of the Bovine Leukemia Virus (BLV) Tax Protein Restricts Transactivation Not Only via the BLV Enhancer but Also via Other Retrovirus Enhancers

PubMed Central

Tajima, Shigeru; Aida, Yoko

2000-01-01

Bovine leukemia virus (BLV) is associated with enzootic bovine leukosis and is closely related to human T-cell leukemia virus type 1 (HTLV-1). The Tax protein of BLV acts through the 5′ long terminal repeat (LTR) of BLV and activates the transcription of BLV. In this study, we amplified tax genes from BLV-infected cattle using PCR. We cloned the genes and monitored the transcriptional activities of the products. Seven independent mutant Tax proteins, with at least one amino acid substitution between residues 240 and 265, exhibited a markedly stronger ability to stimulate the viral LTR-directed transcription than the wild-type Tax protein. Analysis of chimeric Tax proteins derived from wild-type and mutant Tax proteins clearly demonstrated that a single substitution between residue 240 and 265 might be critical for the higher activities of the Tax mutant proteins. Furthermore, it appeared that transient expression of a Tax mutant protein was better able to increase the production of viral proteins and particles from a defective recombinant proviral clone of BLV than was wild-type Tax. Analysis of mutations within the U3 region of the LTR revealed that a cyclic AMP-responsive element in Tax-responsive element 2 might be sufficient for the enhanced activation mediated by the mutant proteins. In addition to the LTR of BLV, other viral enhancers, such as the enhancers of HTLV-1 and of mouse mammary tumor virus, which cannot be activated by wild-type BLV Tax protein, were activated by a Tax mutant protein. Our observations suggest that the transactivation activity and target sequence specificity of BLV Tax might be limited or negatively regulated by the region of the protein between amino acids 240 and 265. PMID:11069988

The tumor marker Fascin is strongly induced by the Tax oncoprotein of HTLV-1 through NF-kappaB signals.

PubMed

Kress, Andrea K; Kalmer, Martina; Rowan, Aileen G; Grassmann, Ralph; Fleckenstein, Bernhard

2011-03-31

Oncogenic transformation of CD4(+) T cells by human T-cell lymphotropic virus type 1 (HTLV-1) is understood as the initial step to adult T-cell leukemia/lymphoma, a process that is mainly initiated by perturbation of cellular signaling by the viral Tax oncoprotein, a potent transcriptional regulator. In search of novel biomarkers with relevance to oncogenesis, we identified the tumor marker and actin-bundling protein Fascin (FSCN1) to be specifically and strongly up-regulated in both HTLV-1-transformed and adult T-cell leukemia/lymphoma patient-derived CD4(+) T cells. Fascin is important for migration and metastasis in various types of cancer. Here we report that a direct link can exist between a single viral oncoprotein and Fascin expression, as the viral oncoprotein Tax was sufficient to induce high levels of Fascin. Nuclear factor-κB signals were important for Tax-mediated transcriptional regulation of Fascin in T cells. This suggests that Fascin up-regulation by Tax contributes to the development of HTLV-1-associated pathogenesis.

Income Tax and the FAFSA for Unaccompanied Homeless Youth

ERIC Educational Resources Information Center

National Association for the Education of Homeless Children and Youth, 2009

2009-01-01

This two-page brief answers various questions about the relationship between the filing of tax returns and a youth's completion of the FAFSA. Questions answered include: How does a youth's decision to file a tax return affect the FAFSA?; Are youth required to file tax returns?; and What should an unaccompanied youth do if his/her parents claim…

17 CFR 256.408 - Taxes other than income taxes.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 17 Commodity and Securities Exchanges 3 2011-04-01 2011-04-01 false Taxes other than income taxes... UTILITY HOLDING COMPANY ACT OF 1935 Income and Expense Accounts § 256.408 Taxes other than income taxes. (a) This account shall include the amount of state unemployment insurance, franchise taxes, federal...

Ternary Complex Factors and Cofactors Are Essential for Human T-Cell Leukemia Virus Type 1 Tax Transactivation of the Serum Response Element

PubMed Central

Shuh, Maureen; Derse, David

2000-01-01

The human T-cell leukemia virus type 1 Tax protein activates the expression of cellular immediate early genes controlled by the serum response element (SRE), which contains both the serum response factor (SRF) binding element (CArG box) and the ternary complex factor (TCF) binding element (Ets box). We show that TCF binding is necessary for Tax activation of the SRE and that Tax directly interacts with TCFs in vitro. In addition, Tax interactions with CREB binding protein (CBP) and p300- and CBP-associated factor were found to be essential for Tax activation of SRF-mediated transcription. PMID:11070040

Molecular evidence that the eukaryotic THO/TREX complex is required for efficient transcription elongation.

PubMed

Rondón, Ana G; Jimeno, Sonia; García-Rubio, María; Aguilera, Andrés

2003-10-03

THO/TREX is a conserved eukaryotic complex formed by the core THO complex plus proteins involved in mRNA metabolism and export such as Sub2 and Yra1. Mutations in any of the THO/TREX structural genes cause pleiotropic phenotypes such as transcription impairment, increased transcription-associated recombination, and mRNA export defects. To assay the relevance of THO/TREX complex in transcription, we performed in vitro transcription elongation assays in mutant cell extracts using supercoiled DNA templates containing two G-less cassettes. With these assays, we demonstrate that hpr1delta, tho2delta, and mft1delta mutants of the THO complex and sub2 mutants show significant reductions in the efficiency of transcription elongation. The mRNA expression defect of hpr1delta mutants was not due to an increase in mRNA decay, as determined by mRNA half-life measurements and mRNA time course accumulation experiments in the absence of Rrp6p exoribonuclease. This work demonstrates that THO and Sub2 are required for efficient transcription elongation, providing further evidence for the coupling between transcription and mRNA metabolism and export.

26 CFR 46.4701-1 - Tax on issuer of registration-required obligation not in registered form.

Code of Federal Regulations, 2010 CFR

2010-04-01

... obligation not in registered form. 46.4701-1 Section 46.4701-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY (CONTINUED) MISCELLANEOUS EXCISE TAXES EXCISE TAX ON POLICIES ISSUED BY FOREIGN INSURERS AND OBLIGATIONS NOT IN REGISTERED FORM Excise Tax on Obligations Not in Registered Form § 46.4701...

The relationship between alcohol taxes and binge drinking: evaluating new tax measures incorporating multiple tax and beverage types.

PubMed

Xuan, Ziming; Chaloupka, Frank J; Blanchette, Jason G; Nguyen, Thien H; Heeren, Timothy C; Nelson, Toben F; Naimi, Timothy S

2015-03-01

U.S. studies contribute heavily to the literature about the tax elasticity of demand for alcohol, and most U.S. studies have relied upon specific excise (volume-based) taxes for beer as a proxy for alcohol taxes. The purpose of this paper was to compare this conventional alcohol tax measure with more comprehensive tax measures (incorporating multiple tax and beverage types) in analyses of the relationship between alcohol taxes and adult binge drinking prevalence in U.S. states. Data on U.S. state excise, ad valorem and sales taxes from 2001 to 2010 were obtained from the Alcohol Policy Information System and other sources. For 510 state-year strata, we developed a series of weighted tax-per-drink measures that incorporated various combinations of tax and beverage types, and related these measures to state-level adult binge drinking prevalence data from the Behavioral Risk Factor Surveillance System surveys. In analyses pooled across all years, models using the combined tax measure explained approximately 20% of state binge drinking prevalence, and documented more negative tax elasticity (-0.09, P = 0.02 versus -0.005, P = 0.63) and price elasticity (-1.40, P < 0.01 versus -0.76, P = 0.15) compared with models using only the volume-based tax. In analyses stratified by year, the R-squares for models using the beer combined tax measure were stable across the study period (P = 0.11), while the R-squares for models rely only on volume-based tax declined (P < 0.0). Compared with volume-based tax measures, combined tax measures (i.e. those incorporating volume-based tax and value-based taxes) yield substantial improvement in model fit and find more negative tax elasticity and price elasticity predicting adult binge drinking prevalence in U.S. states. © 2014 Society for the Study of Addiction.

The relationship between alcohol taxes and binge drinking: evaluating new tax measures incorporating multiple tax and beverage types

PubMed Central

Xuan, Ziming; Chaloupka, Frank J.; Blanchette, Jason G.; Nguyen, Thien H.; Heeren, Timothy C.; Nelson, Toben F.; Naimi, Timothy S.

2015-01-01

Aims U.S. studies contribute heavily to the literature about the tax elasticity of demand for alcohol, and most U.S. studies have relied upon specific excise (volume-based) taxes for beer as a proxy for alcohol taxes. The purpose of this paper was to compare this conventional alcohol tax measure with more comprehensive tax measures (incorporating multiple tax and beverage types) in analyses of the relationship between alcohol taxes and adult binge drinking prevalence in U.S. states. Design Data on U.S. state excise, ad valorem and sales taxes from 2001 to 2010 were obtained from the Alcohol Policy Information System and other sources. For 510 state-year strata, we developed a series of weighted tax-per-drink measures that incorporated various combinations of tax and beverage types, and related these measures to state-level adult binge drinking prevalence data from the Behavioral Risk Factor Surveillance System surveys. Findings In analyses pooled across all years, models using the combined tax measure explained approximately 20% of state binge drinking prevalence, and documented more negative tax elasticity (−0.09, P=0.02 versus −0.005, P=0.63) and price elasticity (−1.40, P<0.01 versus −0.76, P=0.15) compared with models using only the volume-based tax. In analyses stratified by year, the R-squares for models using the beer combined tax measure were stable across the study period (P=0.11), while the R-squares for models rely only on volume-based tax declined (P<0.01). Conclusions Compared with volume-based tax measures, combined tax measures (i.e. those incorporating volume-based tax and value-based taxes) yield substantial improvement in model fit and find more negative tax elasticity and price elasticity predicting adult binge drinking prevalence in U.S. states. PMID:25428795

Tax Tips for Forest Landowners for the 1999 Tax Year

Treesearch

Larry M. Bishop

1999-01-01

Larry Bishop of the USDA Forest Service Southern Region comes through again with conciseinformation to help forest landowners prepare their taxes. Tax Tips for Forest Landowners for the 1999 Tax Year covers basis and tax records; passive loss rules; reforestation tax credit and amortization; capital gains and self-employment taxes; cost-share payments; conservation...

76 FR 13932 - Disclosure of Information to State Officials Regarding Tax-Exempt Organizations

Federal Register 2010, 2011, 2012, 2013, 2014

2011-03-15

... approval of these safeguards by the IRS, as well as satisfaction of any other statutory requirements (such... Employment taxes, Estate taxes, Excise taxes, Gift taxes, Income taxes, Penalties, Reporting and... under section 6104(c) on the ASO's behalf by specifying in writing each person's name and job title, and...

The chaperonin CCTα is required for efficient transcription and replication of rabies virus.

PubMed

Zhang, Jinyang; Ye, Chengjin; Ruan, Xizhen; Zan, Jie; Xu, Yunbin; Liao, Min; Zhou, Jiyong

2014-10-01

Negri bodies (NBs) are formed in the cytoplasm of rabies virus (RABV)-infected cells and are accompanied by a number of host factors to NBs, in which replication and transcription occur. Here, it was found that chaperonin containing TCP-1 subunit alpha (CCTα) relocalizes to NBs in RABV-infected cells, and that cotransfection of nucleo- and phospho-proteins of RABV is sufficient to recruit CCTα to the NBs' structure. Inhibition of CCTα expression by specific short hairpin RNA knockdown inhibited the replication and transcription of RABV. Therefore, this study showed that the host factor CCTα is associated with RABV infection and is very likely required for efficient virus transcription and replication. © 2014 The Societies and Wiley Publishing Asia Pty Ltd.

Is your hospital's tax-exempt status at risk?

PubMed

Ricaud, John S

2006-06-01

The IRS has proposed changes to Section 501(c)(3) of the Internal Revenue Code that could affect the tax-exempt status of not-for-profit healthcare organizations. Healthcare financial managers should ensure that their organizations maintain compliance with the tax-exempt requirements and remain above reproach, particularly in the areas of: An organization's intent for public service. Implications of Section 4958 on the organization's tax-exempt status. Political activities. Operating an affiliated business.

26 CFR 53.4965-7 - Taxes on prohibited tax shelter transactions.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 17 2011-04-01 2011-04-01 false Taxes on prohibited tax shelter transactions... (CONTINUED) MISCELLANEOUS EXCISE TAXES (CONTINUED) FOUNDATION AND SIMILAR EXCISE TAXES Second Tier Excise Taxes § 53.4965-7 Taxes on prohibited tax shelter transactions. (a) Entity-level taxes—(1) In general...

48 CFR 29.401-3 - Federal, State, and local taxes.

Code of Federal Regulations, 2010 CFR

2010-10-01

... 48 Federal Acquisition Regulations System 1 2010-10-01 2010-10-01 false Federal, State, and local... GENERAL CONTRACTING REQUIREMENTS TAXES Contract Clauses 29.401-3 Federal, State, and local taxes. (a... Local Taxes, in solicitations and contracts if— (1) The contract is to be performed wholly or partly in...

77 FR 71481 - Publication of the Tier 2 Tax Rates

Federal Register 2010, 2011, 2012, 2013, 2014

2012-11-30

... DEPARTMENT OF THE TREASURY Internal Revenue Service Publication of the Tier 2 Tax Rates AGENCY... tax rates for calendar year 2013 as required by section 3241(d) of the Internal Revenue Code (26 U.S.C. 3241). Tier 2 taxes on railroad employees, employers, and employee representatives are one source of...

Niclosamide, an anti-helminthic molecule, downregulates the retroviral oncoprotein Tax and pro-survival Bcl-2 proteins in HTLV-1-transformed T lymphocytes

DOE Office of Scientific and Technical Information (OSTI.GOV)

Xiang, Di; Yuan, Yunsheng; Engineering Research Center of Cell and Therapeutic Antibody, Ministry of Education, School of Pharmacy, Shanghai Jiao Tong University, Shanghai

Adult T cell leukemia and lymphoma (ATL) is a highly aggressive form of hematological malignancy and is caused by chronic infection of human T cell leukemia virus type 1 (HTLV-1). The viral genome encodes an oncogenic protein, Tax, which plays a key role in transactivating viral gene transcription and in deregulating cellular oncogenic signaling to promote survival, proliferation and transformation of virally infected T cells. Hence, Tax is a desirable therapeutic target, particularly at early stage of HTLV-1-mediated oncogenesis. We here show that niclosamide, an anti-helminthic molecule, induced apoptosis of HTLV-1-transformed T cells. Niclosamide facilitated degradation of the Tax proteinmore » in proteasome. Consistent with niclosamide-mediated Tax degradation, this compound inhibited activities of MAPK/ERK1/2 and IκB kinases. In addition, niclosamide downregulated Stat3 and pro-survival Bcl-2 family members such as Mcl-1 and repressed the viral gene transcription of HTLV-1 through induction of Tax degradation. Since Tax, Stat3 and Mcl-1 are crucial molecules for promoting survival and growth of HTLV-1-transformed T cells, our findings demonstrate a novel mechanism of niclosamide in inducing Tax degradation and downregulating various cellular pro-survival molecules, thereby promoting apoptosis of HTLV-1-associated leukemia cells. - Highlights: • Niclosamide is a promising therapeutic candidate for adult T cell leukemia. • Niclosamide employs a novel mechanism through proteasomal degradation of Tax. • Niclosamide downregulates certain cellular pro-survival molecules.« less

HTLV Deregulation of the NF-κB Pathway: An Update on Tax and Antisense Proteins Role

PubMed Central

Fochi, Stefania; Mutascio, Simona; Bertazzoni, Umberto; Zipeto, Donato; Romanelli, Maria G.

2018-01-01

Human T-cell lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia (ATL), an aggressive CD4+/CD25+ T-cell malignancy and of a severe neurodegenerative disease, HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). The chronic activation or deregulation of the canonical and non-canonical nuclear factor kappa B (NF-κB) pathways play a crucial role in tumorigenesis. The HTLV-1 Tax-1 oncoprotein is a potent activator of the NF-κB transcription factors and the NF-κB response is required for promoting the development of HTLV-1 transformed cell lines. The homologous retrovirus HTLV-2, which also expresses a Tax-2 transforming protein, is not associated with ATL. In this review, we provide an updated synopsis of the role of Tax-1 in the deregulation of the NF-κB pathway, highlighting the differences with the homologous Tax-2. Special emphasis is directed toward the understanding of the molecular mechanisms involved in NF-κB activation resulting from Tax interaction with host factors affecting several cellular processes, such as cell cycle, apoptosis, senescence, cell proliferation, autophagy, and post-translational modifications. We also discuss the current knowledge on the role of the antisense viral protein HBZ in down-regulating the NF-κB activation induced by Tax, and its implication in cellular senescence. In addition, we review the recent studies on the mechanism of HBZ-mediated inhibition of NF-κB activity as compared to that exerted by the HTLV-2 antisense protein, APH-2. Finally, we discuss recent advances aimed at understanding the role exerted in the development of ATL by the perturbation of NF-κB pathway by viral regulatory proteins. PMID:29515558

HTLV Deregulation of the NF-κB Pathway: An Update on Tax and Antisense Proteins Role.

PubMed

Fochi, Stefania; Mutascio, Simona; Bertazzoni, Umberto; Zipeto, Donato; Romanelli, Maria G

2018-01-01

Human T-cell lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia (ATL), an aggressive CD4 + /CD25 + T-cell malignancy and of a severe neurodegenerative disease, HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). The chronic activation or deregulation of the canonical and non-canonical nuclear factor kappa B (NF-κB) pathways play a crucial role in tumorigenesis. The HTLV-1 Tax-1 oncoprotein is a potent activator of the NF-κB transcription factors and the NF-κB response is required for promoting the development of HTLV-1 transformed cell lines. The homologous retrovirus HTLV-2, which also expresses a Tax-2 transforming protein, is not associated with ATL. In this review, we provide an updated synopsis of the role of Tax-1 in the deregulation of the NF-κB pathway, highlighting the differences with the homologous Tax-2. Special emphasis is directed toward the understanding of the molecular mechanisms involved in NF-κB activation resulting from Tax interaction with host factors affecting several cellular processes, such as cell cycle, apoptosis, senescence, cell proliferation, autophagy, and post-translational modifications. We also discuss the current knowledge on the role of the antisense viral protein HBZ in down-regulating the NF-κB activation induced by Tax, and its implication in cellular senescence. In addition, we review the recent studies on the mechanism of HBZ-mediated inhibition of NF-κB activity as compared to that exerted by the HTLV-2 antisense protein, APH-2. Finally, we discuss recent advances aimed at understanding the role exerted in the development of ATL by the perturbation of NF-κB pathway by viral regulatory proteins.

Interactive Tax Reform: Simulating Impacts of Legislative Proposals.

ERIC Educational Resources Information Center

Downing, Roger H.; And Others

1985-01-01

Pennsylvania's mathematical modeling technique to evaluate tax reform proposals requires the following data: personal income at the local level and measures of the breakdown of property tax payment by land use classification. The simulation technique could be readily adapted in reorganizing educational finance systems. (MLF)

HTLV-1 Tax impairs K63-linked ubiquitination of STING to evade host innate immunity.

PubMed

Wang, Jie; Yang, Shuai; Liu, Lu; Wang, Hui; Yang, Bo

2017-03-15

The cellular antiviral innate immune system is essential for host defense and viruses have evolved a variety of strategies to evade the innate immunity. Human T lymphotropic virus type 1 (HTLV-1) belongs to the deltaretrovirus family and it can establish persistent infection in human beings for many years. However, how this virus evades the host innate immune responses remains unclear. Here we report a new strategy used by HTLV-1 to block innate immune responses. We observed that stimulator of interferon genes (STING) limited HTLV-1 protein expression and was critical to HTLV-1 reverse transcription intermediate (RTI) ssDNA90 triggered interferon (IFN)-β production in phorbol12-myristate13-acetate (PMA)-differentiated THP1 (PMA-THP1) cells. The HTLV-1 protein Tax inhibited STING overexpression induced transcriptional activation of IFN-β. Tax also impaired poly(dA:dT), interferon stimulatory DNA (ISD) or cyclic GMP-AMP (cGAMP) -stimulated IFN-β production, which was dependent on STING activation. Coimmunoprecipitation assays and confocal microscopy indicated that Tax was associated with STING in the same complex. Mechanistic studies suggested that Tax decreased the K63-linked ubiquitination of STING and disrupted the interactions between STING and TANK-binding kinase 1 (TBK1). These findings may shed more light on the molecular mechanisms underlying HTLV-1 infection. Copyright © 2017 Elsevier B.V. All rights reserved.

HTLV-I Tax transrepresses the human c-Myb promoter independently of its interaction with CBP or p300.

PubMed

Nicot, C; Mahieux, R; Opavsky, R; Cereseto, A; Wolff, L; Brady, J N; Franchini, G

2000-04-20

The c-Myb proto-oncogene is preferentially expressed in hematopoietic lineages, and highly expressed in several leukemia types. The Human T-cell Leukemia Virus Type I (HTLV-I) is the etiological agent of Adult T-cell Leukemia/Lymphoma (ATLL). A previous report suggested that Tax, the viral transactivator, is able to suppress the transactivation potential of c-Myb protein by competing for recruitment of CBP. We tested whether such a competition could affect transcription from the c-Myb promoter in Tax expressing T-cells. Using several c-Myb promoter reporter constructs carrying mutations in various regions, we demonstrate that Tax suppression of c-Myb transactivation results in transrepression of the c-Myb promoter through the Myb responsive elements in Jurkat T-cells. The ability of Tax mutants M22, M47 and V89A to interact with the full-length CBP and p300 proteins in vitro, and their ability to repress the c-Myb promoter, was then evaluated. Although both M47 and M22 bind to CBP and p300 to a similar extent, only M47 was able to repress the c-Myb promoter, suggesting that competition for CBP/p300 binding was not the mechanism underlying Tax's effect. This concept was further supported by the fact that the Tax mutant V89A transrepresses the c-Myb promoter efficiently in spite of an impaired binding to CBP and p300. Therefore, Tax-mediated repression of the c-Myb promoter appears to be independent from a direct competition between c-Myb and Tax for recruitment of CBP/p300. Interestingly, a decreased transcription from the endogenous c-Myb promoter was observed in several HTLV-I transformed T-cell lines. Finally, the ability of Tax to directly repress the endogenous c-Myb promoter was demonstrated in a Jurkat cell line stably transfected with a tax gene driven by a cadmium-inducible promoter.

27 CFR 46.233 - Payment of floor stocks tax.

Code of Federal Regulations, 2011 CFR

2011-04-01

... PRODUCTS AND CIGARETTE PAPERS AND TUBES Floor Stocks Tax on Certain Tobacco Products, Cigarette Papers, and Cigarette Tubes Held for Sale on April 1, 2009 Filing Requirements § 46.233 Payment of floor stocks tax. (a...

27 CFR 46.233 - Payment of floor stocks tax.

Code of Federal Regulations, 2010 CFR

2010-04-01

... PRODUCTS AND CIGARETTE PAPERS AND TUBES Floor Stocks Tax on Certain Tobacco Products, Cigarette Papers, and Cigarette Tubes Held for Sale on April 1, 2009 Filing Requirements § 46.233 Payment of floor stocks tax. (a...

27 CFR 46.233 - Payment of floor stocks tax.

Code of Federal Regulations, 2013 CFR

2013-04-01

... PRODUCTS AND CIGARETTE PAPERS AND TUBES Floor Stocks Tax on Certain Tobacco Products, Cigarette Papers, and Cigarette Tubes Held for Sale on April 1, 2009 Filing Requirements § 46.233 Payment of floor stocks tax. (a...

27 CFR 46.233 - Payment of floor stocks tax.

Code of Federal Regulations, 2014 CFR

2014-04-01

... PRODUCTS AND CIGARETTE PAPERS AND TUBES Floor Stocks Tax on Certain Tobacco Products, Cigarette Papers, and Cigarette Tubes Held for Sale on April 1, 2009 Filing Requirements § 46.233 Payment of floor stocks tax. (a...

HTLV-1 Tax transgenic mice develop spontaneous osteolytic bone metastases prevented by osteoclast inhibition

PubMed Central

Gao, Ling; Deng, Hongju; Zhao, Haibo; Hirbe, Angela; Harding, John; Ratner, Lee; Weilbaecher, Katherine

2005-01-01

One in 20 carriers of human T-cell leukemia virus type 1 (HTLV-1) will develop adult T-cell leukemia/lymphoma (ATL), a disease frequently associated with hypercalcemia, bone destruction, and a fatal course refractory to current therapies. Overexpression of the HTLV-1–encoded Tax oncoprotein under the human granzyme B promoter causes large granular lymphocytic leukemia/lymphomas in mice. We found that Tax+ mice spontaneously developed hypercalcemia, high-frequency osteolytic bone metastases, and enhanced osteoclast activity. We evaluated Tax tumors for the production of osteoclast-activating factors. Purification of Tax+ tumor cells and nonmalignant tumor-infiltrating lymphocytes demonstrated that each of these populations expressed transcripts for distinct osteoclast-activating factors. We then evaluated the effect of osteoclast inhibition on tumor formation. Mice doubly transgenic for Tax and the osteoclast inhibitory factor, osteoprotegerin, were protected from osteolytic bone disease and developed fewer soft-tissue tumors. Likewise, osteoclast inhibition with bone-targeted zoledronic acid protected Tax+ mice from bone and soft-tissue tumors and prolonged survival. Tax+ mice represent the first animal model of high-penetrance spontaneous osteolytic bone metastasis and underscore the critical role of nonmalignant host cells recruited by tumor cells in the process of cancer progression and metastasis. PMID:16118323

26 CFR 31.6011(a)-3 - Returns under Federal Unemployment Tax Act.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 15 2010-04-01 2010-04-01 false Returns under Federal Unemployment Tax Act. 31... Provisions of Subtitle F, Internal Revenue Code of 1954) § 31.6011(a)-3 Returns under Federal Unemployment Tax Act. (a) Requirement. Every person shall make a return of tax under the Federal Unemployment Tax...

26 CFR 31.6011(a)-3 - Returns under Federal Unemployment Tax Act.

Code of Federal Regulations, 2012 CFR

2012-04-01

... 26 Internal Revenue 15 2012-04-01 2012-04-01 false Returns under Federal Unemployment Tax Act. 31... Provisions of Subtitle F, Internal Revenue Code of 1954) § 31.6011(a)-3 Returns under Federal Unemployment Tax Act. (a) Requirement. Every person shall make a return of tax under the Federal Unemployment Tax...

26 CFR 31.6011(a)-3 - Returns under Federal Unemployment Tax Act.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 15 2011-04-01 2011-04-01 false Returns under Federal Unemployment Tax Act. 31... Provisions of Subtitle F, Internal Revenue Code of 1954) § 31.6011(a)-3 Returns under Federal Unemployment Tax Act. (a) Requirement. Every person shall make a return of tax under the Federal Unemployment Tax...

26 CFR 31.6011(a)-3 - Returns under Federal Unemployment Tax Act.

Code of Federal Regulations, 2014 CFR

2014-04-01

... 26 Internal Revenue 15 2014-04-01 2014-04-01 false Returns under Federal Unemployment Tax Act. 31... Provisions of Subtitle F, Internal Revenue Code of 1954) § 31.6011(a)-3 Returns under Federal Unemployment Tax Act. (a) Requirement. Every person shall make a return of tax under the Federal Unemployment Tax...

26 CFR 31.6011(a)-3 - Returns under Federal Unemployment Tax Act.

Code of Federal Regulations, 2013 CFR

2013-04-01

... 26 Internal Revenue 15 2013-04-01 2013-04-01 false Returns under Federal Unemployment Tax Act. 31... Provisions of Subtitle F, Internal Revenue Code of 1954) § 31.6011(a)-3 Returns under Federal Unemployment Tax Act. (a) Requirement. Every person shall make a return of tax under the Federal Unemployment Tax...

The Tax Base And The Tax Bill. Tax Implications of Development: A Workbook.

ERIC Educational Resources Information Center

Brighton, Deb; Northup, Jim

The property tax base in Vermont's towns are overburdened as property taxes are usually the only funding method available to finance schools, police departments, highway work, recreation programs, and government in general. Attempting to offer their citizens a balanced program of services without exorbitant taxes, local officials are striving to…

The Impact of IRS Tax Policy on Hospital Community Benefit Activities.

PubMed

Yeager, Valerie A; Ferdinand, Alva O; Menachemi, Nir

2017-04-01

The Internal Revenue Service (IRS) recently introduced tax code revisions requiring stricter oversight of community benefit activities (CBAs) conducted by tax-exempt, not-for-profit hospitals. We examine the impact of this tax requirement on CBAs among these hospitals relative to for-profit and government hospitals that were not subject to the new policy. We employed a quasi-experimental, difference-in-difference study design using a longitudinal observational approach and used secondary data collected by the American Hospital Association (years 2006-2010 including 20,538 hospital year observations). Findings show a significant increase in the reporting of 7 of the 13 CBAs among tax-exempt, not-for-profit hospitals compared with other hospitals after the policy change. Examples include partnering to conduct community health assessments ( b = 0.035, p = .002) and using capacity assessments to identify unmet community health needs ( b = 0.041, p = .001). Recent tax revisions are associated with increases in reported CBAs among tax-exempt, not-for-profit hospitals. As the debate continues regarding tax exemption status for not-for-profit hospitals, policy makers should expand efforts for enhanced accountability.

Discordance between bovine leukemia virus tax immortalization in vitro and oncogenicity in vivo.

PubMed

Twizere, J C; Kerkhofs, P; Burny, A; Portetelle, D; Kettmann, R; Willems, L

2000-11-01

Bovine leukemia virus (BLV) Tax protein, a transcriptional activator of viral expression, is essential for viral replication in vivo. Tax is believed to be involved in leukemogenesis because of its second function, immortalization of primary cells in vitro. These activities of Tax can be dissociated on the basis of point mutations within specific regions of the protein. For example, mutation of the phosphorylation sites at serines 106 and 293 abrogates immortalization potential in vitro but maintains transcriptional activity. This type of mutant is thus particularly useful for unraveling the role of Tax immortalization activity during leukemogenesis independently of viral replication. In this report, we describe the biological properties of BLV recombinant proviruses mutated in the Tax phosphorylation sites (BLVTax106+293). Titration of the proviral loads by semiquantitative PCR revealed that the BLV mutants propagated at wild-type levels in vivo. Furthermore, two animals (sheep 480 and 296) infected with BLVTax106+293 developed leukemia or lymphosarcoma after 16 and 36 months, respectively. These periods of time are within the normal range of latencies preceding the onset of pathogenesis induced by wild-type viruses. The phenotype of the mutant-infected cells was characteristic of a B lymphocyte (immunoglobulin M positive) expressing CD11b and CD5 (except at the final stage for the latter marker), a pattern that is typical of wild-type virus-infected target cells. Interestingly, the transformed B lymphocytes from sheep 480 also coexpressed the CD8 marker, a phenotype rarely observed in tumor biopsies from chronic lymphocytic leukemia patients. Finally, direct sequencing of the tax gene demonstrated that the leukemic cells did not harbor revertant proviruses. We conclude that viruses expressing a Tax mutant unable to transform primary cells in culture are still pathogenic in the sheep animal model. Our data thus provide a clear example of the discordant conclusions

26 CFR 1.853-1 - Foreign tax credit allowed to shareholders.

Code of Federal Regulations, 2012 CFR

2012-04-01

...) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Regulated Investment Companies and Real Estate Investment... regulated investment company, meeting the requirements set forth in section 853(a) and paragraph (b) of this... investment company shall apply their proportionate share of such foreign taxes paid, or deemed to have been...

26 CFR 1.853-1 - Foreign tax credit allowed to shareholders.

Code of Federal Regulations, 2011 CFR

2011-04-01

...) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Regulated Investment Companies and Real Estate Investment... regulated investment company, meeting the requirements set forth in section 853(a) and paragraph (b) of this... investment company shall apply their proportionate share of such foreign taxes paid, or deemed to have been...

26 CFR 1.853-1 - Foreign tax credit allowed to shareholders.

Code of Federal Regulations, 2014 CFR

2014-04-01

...) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Regulated Investment Companies and Real Estate Investment... regulated investment company, meeting the requirements set forth in section 853(a) and paragraph (b) of this... investment company shall apply their proportionate share of such foreign taxes paid, or deemed to have been...

26 CFR 1.853-1 - Foreign tax credit allowed to shareholders.

Code of Federal Regulations, 2013 CFR

2013-04-01

...) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Regulated Investment Companies and Real Estate Investment... regulated investment company, meeting the requirements set forth in section 853(a) and paragraph (b) of this... investment company shall apply their proportionate share of such foreign taxes paid, or deemed to have been...

Health insurance tax credits, the earned income tax credit, and health insurance coverage of single mothers.

PubMed

Cebi, Merve; Woodbury, Stephen A

2014-05-01

The Omnibus Budget Reconciliation Act of 1990 enacted a refundable tax credit for low-income working families who purchased health insurance coverage for their children. This health insurance tax credit (HITC) existed during tax years 1991, 1992, and 1993, and was then rescinded. A difference-in-differences estimator applied to Current Population Survey data suggests that adoption of the HITC, along with accompanying increases in the Earned Income Tax Credit (EITC), was associated with a relative increase of about 4.7 percentage points in the private health insurance coverage of working single mothers with high school or less education. Also, a difference-in-difference-in-differences estimator, which attempts to net out the possible influence of the EITC increases but which requires strong assumptions, suggests that the HITC was responsible for about three-quarters (3.6 percentage points) of the total increase. The latter estimate implies a price elasticity of health insurance take-up of -0.42. Copyright © 2013 John Wiley & Sons, Ltd.

The Calmodulin-Binding Transcription Activator CAMTA1 Is Required for Long-Term Memory Formation in Mice

ERIC Educational Resources Information Center

Bas-Orth, Carlos; Tan, Yan-Wei; Oliveira, Ana M. M.; Bengtson, C. Peter; Bading, Hilmar

2016-01-01

The formation of long-term memory requires signaling from the synapse to the nucleus to mediate neuronal activity-dependent gene transcription. Synapse-to-nucleus communication is initiated by influx of calcium ions through synaptic NMDA receptors and/or L-type voltage-gated calcium channels and involves the activation of transcription factors by…

An interferon regulatory factor binding site in the U5 region of the bovine leukemia virus long terminal repeat stimulates Tax-independent gene expression.

PubMed

Kiermer, V; Van Lint, C; Briclet, D; Vanhulle, C; Kettmann, R; Verdin, E; Burny, A; Droogmans, L

1998-07-01

Bovine leukemia virus (BLV) replication is controlled by both cis- and trans-acting elements. The virus-encoded transactivator, Tax, is necessary for efficient transcription from the BLV promoter, although it is not present during the early stages of infection. Therefore, sequences that control Tax-independent transcription must play an important role in the initiation of viral gene expression. This study demonstrates that the R-U5 sequence of BLV stimulates Tax-independent reporter gene expression directed by the BLV promoter. R-U5 was also stimulatory when inserted immediately downstream from the transcription initiation site of a heterologous promoter. Progressive deletion analysis of this region revealed that a 46-bp element corresponding to the 5' half of U5 is principally responsible for the stimulation. This element exhibited enhancer activity when inserted upstream or downstream from the herpes simplex virus thymidine kinase promoter. This enhancer contains a binding site for the interferon regulatory factors IRF-1 and IRF-2. A 3-bp mutation that destroys the IRF recognition site caused a twofold decrease in Tax-independent BLV long terminal repeat-driven gene expression. These observations suggest that the IRF binding site in the U5 region of BLV plays a role in the initiation of virus replication.

Identification of conserved cis-elements and transcription factors required for sterol-regulated transcription of stearoyl-CoA desaturase 1 and 2.

PubMed

Tabor, D E; Kim, J B; Spiegelman, B M; Edwards, P A

1999-07-16

We previously identified stearoyl-CoA desaturase 2 (SCD2) as a new member of the family of genes that are transcriptionally regulated in response to changing levels of nuclear sterol regulatory element binding proteins (SREBPs) or adipocyte determination and differentiation factor 1 (ADD1). A novel sterol regulatory element (SRE) (5'-AGCAGATTGTG-3') identified in the proximal promoter of the mouse SCD2 gene is required for induction of SCD2 promoter-reporter genes in response to cellular sterol depletion (Tabor, D. E., Kim, J. B., Spiegelman, B. M., and Edwards, P. A. (1998) J. Biol. Chem. 273, 22052-22058). In this report, we demonstrate that this novel SRE is both present in the promoter of the SCD1 gene and is critical for the sterol-dependent transcription of SCD1 promoter-reporter genes. Two conserved cis elements (5'-CCAAT-3') lie 5 and 48 base pairs 3' of the novel SREs in the promoters of both the SCD1 and SCD2 murine genes. Mutation of either of these putative NF-Y binding sites attenuates the transcriptional activation of SCD1 or SCD2 promoter-reporter genes in response to cellular sterol deprivation. Induction of both reporter genes is also attenuated when cells are cotransfected with dominant-negative forms of either NF-Y or SREBP. In addition, we demonstrate that the induction of SCD1 and SCD2 mRNAs that occurs during the differentiation of 3T3-L1 preadipocytes to adipocytes is paralleled by an increase in the levels of ADD1/SREBP-1c and that the SCD1 and SCD2 mRNAs are induced to even higher levels in response to ectopic expression of ADD1/SREBP-1c. We conclude that transcription of both SCD1 and SCD2 genes is responsive to cellular sterol levels and to the levels of nuclear SREBP/ADD1 and that transcriptional induction requires three spatially conserved cis elements, that bind SREBP and NF-Y. Additional studies demonstrate that maximal transcriptional repression of SCD2 reporter genes in response to an exogenous polyunsaturated fatty acid is

26 CFR 31.6302-1T - Federal tax deposit rules for withheld income taxes and taxes under the Federal Insurance...

Code of Federal Regulations, 2010 CFR

2010-04-01

... taxes and taxes under the Federal Insurance Contributions Act (FICA) attributable to payments made after..., DEPARTMENT OF THE TREASURY (CONTINUED) EMPLOYMENT TAXES AND COLLECTION OF INCOME TAX AT SOURCE EMPLOYMENT TAXES AND COLLECTION OF INCOME TAX AT SOURCE Administrative Provisions of Special Application to...

24 CFR 599.507 - Tax incentives utilization plan.

Code of Federal Regulations, 2011 CFR

2011-04-01

... utilization plan for achieving the State and local commitments made at the time of application as required by... 24 Housing and Urban Development 3 2011-04-01 2010-04-01 true Tax incentives utilization plan. 599....507 Tax incentives utilization plan. (a) Preliminary plan. Within six months of designation, the CoRA...

Tax tips for forest landowners for the 2008 tax year

Treesearch

Linda Wang; John L. Greene

2009-01-01

This article summarizes key federal income tax provisions for forestland owners, foresters, loggers, forest product businesses, and tax practioners, and is current as of October 1, 2008.  Consult your tax and legal professionals for advice on your particular tax situation.

26 CFR 31.6302-1 - Federal tax deposit rules for withheld income taxes and taxes under the Federal Insurance...

Code of Federal Regulations, 2010 CFR

2010-04-01

... withheld income taxes and taxes under the Federal Insurance Contributions Act (FICA) attributable to... 3405; and (iv) The income tax withheld under section 3406, relating to backup withholding with respect... taxes and taxes under the Federal Insurance Contributions Act (FICA) attributable to payments made after...

An Exposed KID-Like Domain in Human T-Cell Lymphotropic Virus Type 1 Tax Is Responsible for the Recruitment of Coactivators CBP/p300

PubMed Central

Harrod, Robert; Tang, Yong; Nicot, Christophe; Lu, Hsieng S.; Vassilev, Alex; Nakatani, Yoshihiro; Giam, Chou-Zen

1998-01-01

Human T-cell lymphotropic virus type 1 (HTLV-1) transcriptional activation is mediated by the viral transactivator, Tax, and three 21-bp repeats (Tax response element [TxRE]) located in the U3 region of the viral long terminal repeat (LTR). Each TxRE contains a core cyclic AMP response element (CRE) flanked by 5′ G-rich and 3′ C-rich sequences. The TxRE binds CREB (CRE-binding protein) and Tax to form a ternary complex and confers Tax-dependent transactivation. Recent data indicate that Tax functions as a specific link to connect CREB-binding protein (CBP)/p300 in a phosphorylation-independent manner to CREB/ATF-1 assembled on the viral 21-bp repeats. Glutathione S-transferase pull-down performed with Tax deletion mutants and peptide competition have localized the site in Tax critical for binding CBP/p300 to a highly protease-sensitive region around amino acid residues 81 to 95 (81QRTSKTLKVLTPPIT95) which lies between the domains previously proposed to be important for CREB binding and Tax subunit dimerization. Amino acid residues around the trypsin- and chymotrypsin-sensitive sites (88KVL90) of Tax bear resemblance to those in the kinase-inducible domain of CREB (129SRRPSYRKILNE140) surrounding Ser-133, which undergoes signal-induced phosphorylation to recruit CBP/p300. Site-directed mutagenesis of residues in this domain (R82A, K85A, K88A, and V89A) resulted in proteins which failed to transactivate from the HTLV-1 LTR in vivo. These mutants (K85A, K88A, and V89A) bind CREB with similar affinities as wild-type Tax, yet interaction with CBP/p300 is abrogated in various biochemical assays, indicating that the recruitment of CBP/p300 is crucial for Tax transactivation. A Tax mutant, M47, defective in the COOH-terminal transactivation domain, continued to interact with CBP/p300, suggesting that interactions with additional cellular factors are required for proper Tax function. PMID:9710589

The MHC-II transactivator CIITA, a restriction factor against oncogenic HTLV-1 and HTLV-2 retroviruses: similarities and differences in the inhibition of Tax-1 and Tax-2 viral transactivators

PubMed Central

Forlani, Greta; Abdallah, Rawan; Accolla, Roberto S.; Tosi, Giovanna

2013-01-01

The activation of CD4+ T helper cells is strictly dependent on the presentation of antigenic peptides by MHC class II (MHC-II) molecules. MHC-II expression is primarily regulated at the transcriptional level by the AIR-1 gene product CIITA (class II transactivator). Thus, CIITA plays a pivotal role in the triggering of the adaptive immune response against pathogens. Besides this well known function, we recently found that CIITA acts as an endogenous restriction factor against HTLV-1 (human T cell lymphotropic virus type 1) and HTLV-2 oncogenic retroviruses by targeting their viral transactivators Tax-1 and Tax-2, respectively. Here we review our findings on CIITA-mediated inhibition of viral replication and discuss similarities and differences in the molecular mechanisms by which CIITA specifically counteracts the function of Tax-1 and Tax-2 molecules. The dual function of CIITA as a key regulator of adaptive and intrinsic immunity represents a rather unique example of adaptation of host-derived factors against pathogen infections during evolution. PMID:23986750

29 CFR 794.121 - Exclusion of excise taxes.

Code of Federal Regulations, 2010 CFR

2010-07-01

... From Overtime Pay Requirements Under Section 7(b)(3) of the Act Annual Gross Volume of Sales § 794.121 Exclusion of excise taxes. The computation of the annual gross volume of sales of the enterprise for... excise taxes which are included in the sales price may be excluded in computing the annual gross volume...

Activation of the Transcription Factor NF-[Kappa]B by Retrieval Is Required for Long-Term Memory Reconsolidation

ERIC Educational Resources Information Center

Maldonado, Hector; Romano, Arturo; Merlo, Emiliano; Freudenthal, Ramiro

2005-01-01

Several studies support that stored memories undergo a new period of consolidation after retrieval. It is not known whether this process, termed reconsolidation, requires the same transcriptional mechanisms involved in consolidation. Increasing evidence supports the participation of the transcription factor NF-[Kappa]B in memory. This was…

The Spanish tobacco tax loopholes and their consequences.

PubMed

López-Nicolás, Ángel; Cobacho, María Belén; Fernández, Esteve

2013-05-01

The Spanish government has strengthened tobacco control policies since 2005, including changes in tobacco taxes. Because these changes have targeted cigarettes mainly, the tobacco industry has marketed cheaper alternative tobacco products, offering smokers the possibility to downtrade. This paper traces the evolution of patterns of demand for cigarettes and other tobacco products in Spain over the period 2005-2011 in order to assess the impact of such tax loopholes. The authors use data on tobacco products prices and sales as well as changes in the structure and levels of tobacco taxes to relate tax changes to price changes and subsequent market share changes. Tax reforms have lifted the bottom end of the cigarette price distribution, but the industry has been successful in marketing fine-cut tobacco at cheap prices. There have been partial attempts to correct this asymmetric tax treatment, but these have not avoided a remarkable increase in the market share of fine-cut tobacco. The absence of a minimum tax on quantity for the rest of tobacco products allows the industry to place them as potential future downtrading vehicles. In order to address public health objectives, tax policies should aim to equalise the cost of smoking across different tobacco products. Otherwise the tobacco industry can exploit tax loopholes to market cheap alternatives to cigarettes. This requires all tobacco products to bear a minimum tax on quantity, whose levels need to be adjusted in order to reflect the equivalence between different forms of smoking.

75 FR 51914 - Prohibition of the Escrowing of Tax Credit Equity

Federal Register 2010, 2011, 2012, 2013, 2014

2010-08-23

... of Tax Credit Equity; Final Rule #0;#0;Federal Register / Vol. 75 , No. 162 / Monday, August 23, 2010... [Docket No. FR-5290-F-02] RIN 2502-AI73 Prohibition of the Escrowing of Tax Credit Equity AGENCY: Office... requirement that tax credit sales proceeds be placed into escrow, at the time of initial endorsement, for...

26 CFR 1.6161-1 - Extension of time for paying tax or deficiency.

Code of Federal Regulations, 2010 CFR

2010-04-01

... tax is required to be paid to the Director of International Operations, such application must be filed... 26 Internal Revenue 13 2010-04-01 2010-04-01 false Extension of time for paying tax or deficiency... (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES Extensions of Time for Payment § 1.6161-1 Extension of time...

26 CFR 1.641(a)-1 - Imposition of tax; application of tax.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 8 2010-04-01 2010-04-01 false Imposition of tax; application of tax. 1.641(a... (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES Estates, Trusts, and Beneficiaries § 1.641(a)-1 Imposition of tax; application of tax. For taxable years beginning after December 31, 1970, section 641 prescribes...

26 CFR 1.903-1 - Taxes in lieu of income taxes.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 9 2011-04-01 2011-04-01 false Taxes in lieu of income taxes. 1.903-1 Section 1.903-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Income from Sources Without the United States § 1.903-1 Taxes in lieu of...

26 CFR 1.511-4 - Minimum tax for tax preferences.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 7 2010-04-01 2010-04-01 true Minimum tax for tax preferences. 1.511-4 Section 1.511-4 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Taxation of Business Income of Certain Exempt Organizations § 1.511-4...

26 CFR 1.511-4 - Minimum tax for tax preferences.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 7 2011-04-01 2009-04-01 true Minimum tax for tax preferences. 1.511-4 Section 1.511-4 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Taxation of Business Income of Certain Exempt Organizations § 1.511-4...

26 CFR 1.903-1 - Taxes in lieu of income taxes.

Code of Federal Regulations, 2010 CFR

2010-04-01

... taxes. (a) In general. Section 903 provides that the term “income, war profits, and excess profits taxes” shall include a tax paid in lieu of a tax on income, war profits, or excess profits (“income tax... X currency) but is allowed a credit for 30u of excise tax that it has paid. Pursuant to paragraph (e...

26 CFR 157.6161-1 - Extension of time for paying tax.

Code of Federal Regulations, 2010 CFR

2010-04-01

...) MISCELLANEOUS EXCISE TAXES (CONTINUED) EXCISE TAX ON STRUCTURED SETTLEMENT FACTORING TRANSACTIONS Procedure and... Factoring Transactions) of the Internal Revenue Code and shown or required to be shown on any return. The...

POB3 is required for both transcription and replication in the yeast Saccharomyces cerevisiae.

PubMed Central

Schlesinger, M B; Formosa, T

2000-01-01

Spt16 and Pob3 form stable heterodimers in Saccharomyces cerevisiae, and homologous proteins have also been purified as complexes from diverse eukaryotes. This conserved factor has been implicated in both transcription and replication and may affect both by altering the characteristics of chromatin. Here we describe the isolation and properties of a set of pob3 mutants and confirm that they have defects in both replication and transcription. Mutation of POB3 caused the Spt(-) phenotype, spt16 and pob3 alleles displayed severe synthetic defects, and elevated levels of Pob3 suppressed some spt16 phenotypes. These results are consistent with previous reports that Spt16 and Pob3 act in a complex that modulates transcription. Additional genetic interactions were observed between pob3 mutations and the genes encoding several DNA replication factors, including POL1, CTF4, DNA2, and CHL12. pob3 alleles caused sensitivity to the ribonucleotide reductase inhibitor hydroxyurea, indicating a defect in a process requiring rapid dNTP synthesis. Mutation of the S phase checkpoint gene MEC1 caused pob3 mutants to lose viability rapidly under restrictive conditions, revealing defects in a process monitored by Mec1. Direct examination of DNA contents by flow cytometry showed that S phase onset and progression were delayed when POB3 was mutated. We conclude that Pob3 is required for normal replication as well as for transcription. PMID:10924459

78 FR 75471 - Section 3504 Agent Employment Tax Liability

Federal Register 2010, 2011, 2012, 2013, 2014

2013-12-12

... under section 3504 of the Internal Revenue Code to perform acts required of employers who are home care... home care services, which are subject to taxes under the Federal Unemployment Tax Act. The final... amendments to the existing regulatory language designed to update citations and be consistent with the...

42 CFR 433.68 - Permissible health care-related taxes.

Code of Federal Regulations, 2012 CFR

2012-10-01

... 42 Public Health 4 2012-10-01 2012-10-01 false Permissible health care-related taxes. 433.68 Section 433.68 Public Health CENTERS FOR MEDICARE & MEDICAID SERVICES, DEPARTMENT OF HEALTH AND HUMAN... Requirements State Financial Participation § 433.68 Permissible health care-related taxes. (a) General rule. A...

42 CFR 433.68 - Permissible health care-related taxes.

Code of Federal Regulations, 2014 CFR

2014-10-01

... 42 Public Health 4 2014-10-01 2014-10-01 false Permissible health care-related taxes. 433.68 Section 433.68 Public Health CENTERS FOR MEDICARE & MEDICAID SERVICES, DEPARTMENT OF HEALTH AND HUMAN... Requirements State Financial Participation § 433.68 Permissible health care-related taxes. (a) General rule. A...

President Carter signs $227 billion excise tax measure

DOE Office of Scientific and Technical Information (OSTI.GOV)

Miller, C.J.; McAfee, J.; Dibona, C.J.

1980-04-07

According to President J. Carter, who signed into law a $227 billion excise tax (windfall profits tax) on revenue from decontrolled U.S. crude oil production, the new tax program will provide the U.S. with the incentive and the means to produce and conserve domestic oil and replace more oil with alternative sources of energy. According to C. DiBona (API), the new tax will discourage the increased amount of domestic production required to compensate, by the mid-to-late 1980's, for a 1.7 million bbl/day shortfall, which will have to be made up with imports from foreign producers. According to J. McAfee ofmore » Gulf Oil Corp., only a token amount, about $34 billion of the $227 billion which will be raised by the new tax over the next decade, will be devoted to energy development and mass transit. According to C. J. Miller of the Independent Petroleum Association of America, the tax's complex and sometimes conflicting regulations will pose harsh problems for smaller producers.« less

Acetylation of the human T-cell leukemia virus type 1 Tax oncoprotein by p300 promotes activation of the NF-{kappa}B pathway

DOE Office of Scientific and Technical Information (OSTI.GOV)

Lodewick, Julie; Lamsoul, Isabelle; Polania, Angela

The oncogenic potential of the HTLV-1 Tax protein involves activation of the NF-{kappa}B pathway, which depends on Tax phosphorylation, ubiquitination and sumoylation. We demonstrate that the nuclei of Tax-expressing cells, including HTLV-1 transformed T-lymphocytes, contain a pool of Tax molecules acetylated on lysine residue at amino acid position 346 by the transcriptional coactivator p300. Phosphorylation of Tax on serine residues 300/301 was a prerequisite for Tax localization in the nucleus and correlated with its subsequent acetylation by p300, whereas sumoylation, resulting in the formation of Tax nuclear bodies in which p300 was recruited, favored Tax acetylation. Overexpression of p300 markedlymore » increased Tax acetylation and the ability of a wild type HTLV-1 provirus, -but not of a mutant provirus carrying an acetylation deficient Tax gene-, to activate gene expression from an integrated NF-{kappa}B-controlled promoter. Thus, Tax acetylation favors NF-{kappa}B activation and might play an important role in HTLV-1-induced cell transformation.« less

The transcriptional coactivator Maml1 is required for Notch2-mediated marginal zone B-cell development

PubMed Central

Maillard, Ivan; Nakamura, Makoto; Pear, Warren S.; Griffin, James D.

2007-01-01

Signaling mediated by various Notch receptors and their ligands regulates diverse biological processes, including lymphoid cell fate decisions. Notch1 is required during T-cell development, while Notch2 and the Notch ligand Delta-like1 control marginal zone B (MZB) cell development. We previously determined that Mastermind-like (MAML) transcriptional coactivators are required for Notchinduced transcription by forming ternary nuclear complexes with Notch and the transcription factor CSL. The 3 MAML family members (MAML1-MAML3) are collectively essential for Notch activity in vivo, but whether individual MAMLs contribute to the specificity of Notch functions is unknown. Here, we addressed this question by studying lymphopoiesis in the absence of the Maml1 gene. Since Maml1−/− mice suffered perinatal lethality, hematopoietic chimeras were generated with Maml1−/−, Maml1+/−, or wild-type fetal liver progenitors. Maml1 deficiency minimally affected T-cell development, but was required for the development of MZB cells, similar to the phenotype of Notch2 deficiency. Moreover, the number of MZB cells correlated with Maml1 gene dosage. Since all 3 Maml genes were expressed in MZB cells and their precursors, these results suggest that Maml1 is specifically required for Notch2 signaling in MZB cells. PMID:17699740

27 CFR 70.411 - Imposition of taxes, qualification requirements, and regulations.

Code of Federal Regulations, 2012 CFR

2012-04-01

... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Imposition of taxes... from label approval. (14) Establishment and operations of breweries and experimental breweries. Part 25... the ownership, control, and management thereof, and the establishment and operations of experimental...

Tax tips for forest landowners for the 2009 tax year

Treesearch

Linda Wang; John Greene

2010-01-01

This bulletin summarizes federal income tax information useful to woodland owners in preparing their 2009 tax returns. It is current as of October 1, 2009, and supersedes Management Bulletin R8-MB 132. It should not be sonstrued as legal or accounting advice: consult your legal and tax professionals for advice on your particular tax situation.

Arginine Transcriptional Response Does Not Require Inositol Phosphate Synthesis*

PubMed Central

Bosch, Daniel; Saiardi, Adolfo

2012-01-01

Inositol phosphates are key signaling molecules affecting a large variety of cellular processes. Inositol-polyphosphate multikinase (IPMK) is a central component of the inositol phosphate biosynthetic routes, playing essential roles during development. IPMK phosphorylates inositol 1,4,5-trisphosphate to inositol tetrakisphosphate and subsequently to inositol pentakisphosphate and has also been described to function as a lipid kinase. Recently, a catalytically inactive mammalian IPMK was reported to be involved in nutrient signaling by way of mammalian target of rapamycin and AMP-activated protein kinase. In yeast, the IPMK homologue, Arg82, is the sole inositol-trisphosphate kinase. Arg82 has been extensively studied as part of the transcriptional complex regulating nitrogen sensing, in particular arginine metabolism. Whether this role requires Arg82 catalytic activity has long been a matter of contention. In this study, we developed a novel method for the real time study of promoter strength in vivo and used it to demonstrate that catalytically inactive Arg82 fully restored the arginine-dependent transcriptional response. We also showed that expression in yeast of catalytically active, but structurally very different, mammalian or plant IPMK homologue failed to restore arginine regulation. Our work indicates that inositol phosphates do not regulate arginine-dependent gene expression. PMID:22992733

Nuclear Export and Expression of Human T-Cell Leukemia Virus Type 1 tax/rex mRNA Are RxRE/Rex Dependent

PubMed Central

Bai, X. T.; Sinha-Datta, U.; Ko, N. L.; Bellon, M.

2012-01-01

Human T-cell leukemia virus type 1 (HTLV-1) is a complex retrovirus associated with the lymphoproliferative disease adult T-cell leukemia/lymphoma (ATL) and the neurodegenerative disorder tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM). Replication of HTLV-1 is under the control of two major trans-acting proteins, Tax and Rex. Previous studies suggested that Tax activates transcription from the viral long terminal repeat (LTR) through recruitment of cellular CREB and transcriptional coactivators. Other studies reported that Rex acts posttranscriptionally and allows the cytoplasmic export of unspliced or incompletely spliced viral mRNAs carrying gag/pol and env only. As opposed to HIV's Rev-responsive element (RRE), the Rex-responsive element (RxRE) is present in all viral mRNAs in HTLV-1. However, based on indirect observations, it is believed that nuclear export and expression of the doubly spliced tax/rex RNA are Rex independent. In this study, we demonstrate that Rex does stimulate Tax expression, through nuclear-cytoplasmic export of the tax/rex RNA, even though a Rex-independent basal export mechanism exists. This effect was dependent upon the RxRE element and the RNA-binding activity of Rex. In addition, Rex-mediated export of tax/rex RNA was CRM1 dependent and inhibited by leptomycin B treatment. RNA immunoprecipitation (RNA-IP) experiments confirmed Rex binding to the tax/rex RNA in both transfected cells with HTLV-1 molecular clones and HTLV-1-infected T cells. Since both Rex and p30 interact with the tax/rex RNA and with one another, this may offer a temporal and dynamic regulation of HTLV-1 replication. Our results shed light on HTLV-1 replication and reveal a more complex regulatory network than previously anticipated. PMID:22318152

Taxing Situations.

ERIC Educational Resources Information Center

Sabo, Sandra R.

1995-01-01

This article reviews the tax implications of alumni association merchandising programs, focusing on unrelated business income tax (UBIT) that nonprofit organizations, such as alumni associations, must pay on income derived from a trade or business not substantially related to their tax-exempt status. It also discusses postal regulations that…

HTLV-1 Tax Mediated Downregulation of miRNAs Associated with Chromatin Remodeling Factors in T Cells with Stably Integrated Viral Promoter

PubMed Central

Rahman, Saifur; Quann, Kevin; Pandya, Devanshi; Singh, Shruti; Khan, Zafar K.; Jain, Pooja

2012-01-01

RNA interference (RNAi) is a natural cellular mechanism to silence gene expression and is predominantly mediated by microRNAs (miRNAs) that target messenger RNA. Viruses can manipulate the cellular processes necessary for their replication by targeting the host RNAi machinery. This study explores the effect of human T-cell leukemia virus type 1 (HTLV-1) transactivating protein Tax on the RNAi pathway in the context of a chromosomally integrated viral long terminal repeat (LTR) using a CD4+ T-cell line, Jurkat. Transcription factor profiling of the HTLV-1 LTR stably integrated T-cell clone transfected with Tax demonstrates increased activation of substrates and factors associated with chromatin remodeling complexes. Using a miRNA microarray and bioinformatics experimental approach, Tax was also shown to downregulate the expression of miRNAs associated with the translational regulation of factors required for chromatin remodeling. These observations were validated with selected miRNAs and an HTLV-1 infected T cells line, MT-2. miR-149 and miR-873 were found to be capable of directly targeting p300 and p/CAF, chromatin remodeling factors known to play critical role in HTLV-1 pathogenesis. Overall, these results are first in line establishing HTLV-1/Tax-miRNA-chromatin concept and open new avenues toward understanding retroviral latency and/or replication in a given cell type. PMID:22496815

Limited take-up of health coverage tax credits: a challenge to future tax credit design.

PubMed

Dorn, Stan; Varon, Janet; Pervez, Fouad

2005-10-01

The Trade Act of 2002 created federal tax credits to subsidize health coverage for certain early retirees and workers displaced by international trade. Though small, this program offers the opportunity to learn how to design future tax credits for larger groups of uninsured. During September 2004, the most recent month for which there are data about all forms of Trade Act credits, roughly 22 percent of eligible individuals received credits. The authors find that health insurance tax credits are more likely to reach their target populations if such credits: 1) limit premium costs for the low-income uninsured and do not require full premium payments while applications are pending; 2) provide access to coverage that beneficiaries value, including care for preexisting conditions; 3) are combined with outreach that uses easily understandable, multilingual materials and proactive enrollment efforts; and 4) feature a simple application process involving one form filed with one agency.

Requirements for selective recruitment of Ets proteins and activation of mb-1/Ig-α gene transcription by Pax-5 (BSAP)

PubMed Central

Maier, Holly; Ostraat, Rachel; Parenti, Sarah; Fitzsimmons, Daniel; Abraham, Lawrence J.; Garvie, Colin W.; Hagman, James

2003-01-01

Pax-5, a member of the paired domain family of transcription factors, is a key regulator of B lymphocyte-specific transcription and differentiation. A major target of Pax-5-mediated activation is the mb-1 gene, which encodes the essential transmembrane signaling protein Ig-α. Pax-5 recruits three members of the Ets family of transcription factors: Ets-1, Fli-1 and GABPα (with GABPβ1), to assemble ternary complexes on the mb-1 promoter in vitro. Using the Pax-5:Ets-1:DNA crystal structure as a guide, we defined amino acid requirements for transcriptional activation of endogenous mb-1 genes using a novel cell-based assay. Mutations in the β-hairpin/β-turn of the DNA-binding domain of Pax-5 demonstrated its importance for DNA sequence recognition and activation of mb-1 transcription. Mutations of amino acids contacting Ets-1 in the crystal structure reduced or blocked mb-1 promoter activation. One of these mutations, Q22A, resulted in greatly reduced mb-1 gene transcript levels, concurrent with the loss of its ability to recruit Fli-1 to bind the promoter in vitro. In contrast, the mutation had no effect on recruitment of the related Ets protein GABPα (with GABPβ1). These data further define requirements for Pax-5 function in vivo and reveal the complexity of interactions required for cooperative partnerships between transcription factors. PMID:14500810

Employment Security Tax

Science.gov Websites

Alaska > DOLWD > Employment Security Tax EMAIL SCAM ALERT (December 2012) On-line Employer Services Online Filing Demonstrations FAQs for TaxWeb Employer Report Notice Alaska Unemployment Insurance Tax Handbook The Employment Security Tax Section is responsible for providing assistance and information to

Credits and Exemptions for Children. Tax Facts from the Tax Policy Center. Tax Notes[R

ERIC Educational Resources Information Center

Maag, Elaine

2009-01-01

The Earned Income Tax Credit, Child Tax Credit (CTC), Additional Child Tax Credit (ACTC), and the dependent exemption all provide benefits to families with children. In 2009, a single mom (or dad) with two children can receive benefits ranging from $0 to about $7,500--depending on her income, age of the children, and where the children live. While…

26 CFR 1.905-4T - Notification of foreign tax redetermination (temporary).

Code of Federal Regulations, 2010 CFR

2010-04-01

... redetermination of United States tax liability is required occurs after the date for providing such notification... not paid before the date two years after the close of the taxable year to which such taxes relate, the... undistributed earnings and post-1986 foreign income taxes before and after adjusting the pools in accordance...

26 CFR 1.857-4 - Tax imposed by reason of the failure to meet certain source-of-income requirements.

Code of Federal Regulations, 2011 CFR

2011-04-01

..., DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Real Estate Investment.... Section 857(b)(5) imposes a tax on a real estate investment trust that is considered, by reason of section...

26 CFR 1.857-4 - Tax imposed by reason of the failure to meet certain source-of-income requirements.

Code of Federal Regulations, 2012 CFR

2012-04-01

..., DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Real Estate Investment.... Section 857(b)(5) imposes a tax on a real estate investment trust that is considered, by reason of section...

26 CFR 1.857-4 - Tax imposed by reason of the failure to meet certain source-of-income requirements.

Code of Federal Regulations, 2013 CFR

2013-04-01

..., DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Real Estate Investment.... Section 857(b)(5) imposes a tax on a real estate investment trust that is considered, by reason of section...

26 CFR 1.857-4 - Tax imposed by reason of the failure to meet certain source-of-income requirements.

Code of Federal Regulations, 2014 CFR

2014-04-01

..., DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Real Estate Investment.... Section 857(b)(5) imposes a tax on a real estate investment trust that is considered, by reason of section...

Unexpected sequences and structures of mtDNA required for efficient transcription from the first heavy-strand promoter

PubMed Central

Uchida, Akira; Murugesapillai, Divakaran; Kastner, Markus; Wang, Yao; Lodeiro, Maria F; Prabhakar, Shaan; Oliver, Guinevere V; Arnold, Jamie J; Maher, L James; Williams, Mark C; Cameron, Craig E

2017-01-01

Human mtDNA contains three promoters, suggesting a need for differential expression of the mitochondrial genome. Studies of mitochondrial transcription have used a reductionist approach, perhaps masking differential regulation. Here we evaluate transcription from light-strand (LSP) and heavy-strand (HSP1) promoters using templates that mimic their natural context. These studies reveal sequences upstream, hypervariable in the human population (HVR3), and downstream of the HSP1 transcription start site required for maximal yield. The carboxy-terminal tail of TFAM is essential for activation of HSP1 but not LSP. Images of the template obtained by atomic force microscopy show that TFAM creates loops in a discrete region, the formation of which correlates with activation of HSP1; looping is lost in tail-deleted TFAM. Identification of HVR3 as a transcriptional regulatory element may contribute to between-individual variability in mitochondrial gene expression. The unique requirement of HSP1 for the TFAM tail may enable its regulation by post-translational modifications. DOI: http://dx.doi.org/10.7554/eLife.27283.001 PMID:28745586

Taxing energy

DOE Office of Scientific and Technical Information (OSTI.GOV)

Deacon, R.; DeCanio, S.; Frech, H.E. III

1990-01-01

In this book, the authors have produced an analysis of state energy taxation. Their factual findings are of particular relevance to California and other states in their consideration of severance taxes on oil production. It turns out, for example, that while California's tax burden on oil producers is slightly below average among the states, the combined revenues from taxes and royalties (expressed as a percent of the value of production) indicate that California is not easy on oil producers. In fact, California's oil tax system appears to be particularly well suited to its oil industry. Much of the production inmore » the state is relatively high-cost and economically marginal. The state must tread carefully in taxing this production, lest it force it to be curtailed.« less

Direct inhibition of RNAse T2 expression by the HTLV-1 viral protein Tax.

PubMed

Polakowski, Nicholas; Han, Hongjin; Lemasson, Isabelle

2011-08-01

Adult T-cell leukemia (ATL) is one of the primary diseases caused by Human T-cell Leukemia Virus type 1 (HTLV-1) infection. The virally-encoded Tax protein is believed to initiate early events in the development of this disease, as it is able to promote immortalization of T-cells and transformation of other cell types. These processes may be aided by the ability of the viral protein to directly deregulate expression of specific cellular genes through interactions with numerous transcriptional regulators. To identify gene promoters where Tax is localized, we isolated Tax-DNA complexes from an HTLV-1-infected T-cell line through a chromatin immunoprecipitation (ChIP) assay and used the DNA to probe a CpG island microarray. A site within the RNASET2 gene was found to be occupied by Tax. Real-time PCR analysis confirmed this result, and transient expression of Tax in uninfected cells led to the recruitment of the viral protein to the promoter. This event correlated with a decrease in the level of RNase T2 mRNA and protein, suggesting that Tax represses expression of this gene. Loss of RNase T2 expression occurs in certain hematological malignancies and other forms of cancer, and RNase T2 was recently reported to function as a tumor suppressor. Consequently, a reduction in the level of RNase T2 by Tax may play a role in ATL development.

Direct Inhibition of RNAse T2 Expression by the HTLV-1 Viral Protein Tax

PubMed Central

Polakowski, Nicholas; Han, Hongjin; Lemasson, Isabelle

2011-01-01

Adult T-cell leukemia (ATL) is one of the primary diseases caused by Human T-cell Leukemia Virus type 1 (HTLV-1) infection. The virally-encoded Tax protein is believed to initiate early events in the development of this disease, as it is able to promote immortalization of T-cells and transformation of other cell types. These processes may be aided by the ability of the viral protein to directly deregulate expression of specific cellular genes through interactions with numerous transcriptional regulators. To identify gene promoters where Tax is localized, we isolated Tax-DNA complexes from an HTLV-1-infected T-cell line through a chromatin immunoprecipitation (ChIP) assay and used the DNA to probe a CpG island microarray. A site within the RNASET2 gene was found to be occupied by Tax. Real-time PCR analysis confirmed this result, and transient expression of Tax in uninfected cells led to the recruitment of the viral protein to the promoter. This event correlated with a decrease in the level of RNase T2 mRNA and protein, suggesting that Tax represses expression of this gene. Loss of RNase T2 expression occurs in certain hematological malignancies and other forms of cancer, and RNase T2 was recently reported to function as a tumor suppressor. Consequently, a reduction in the level of RNase T2 by Tax may play a role in ATL development. PMID:21994792

26 CFR 1.164-5 - Certain retail sales taxes and gasoline taxes.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 2 2011-04-01 2011-04-01 false Certain retail sales taxes and gasoline taxes. 1....164-5 Certain retail sales taxes and gasoline taxes. For taxable years beginning before January 1...) and tax on the sale of gasoline, diesel fuel or other motor fuel paid by the consumer (other than in...

26 CFR 1.164-5 - Certain retail sales taxes and gasoline taxes.

Code of Federal Regulations, 2013 CFR

2013-04-01

... 26 Internal Revenue 2 2013-04-01 2013-04-01 false Certain retail sales taxes and gasoline taxes. 1....164-5 Certain retail sales taxes and gasoline taxes. For taxable years beginning before January 1...) and tax on the sale of gasoline, diesel fuel or other motor fuel paid by the consumer (other than in...

26 CFR 1.164-5 - Certain retail sales taxes and gasoline taxes.

Code of Federal Regulations, 2012 CFR

2012-04-01

... 26 Internal Revenue 2 2012-04-01 2012-04-01 false Certain retail sales taxes and gasoline taxes. 1....164-5 Certain retail sales taxes and gasoline taxes. For taxable years beginning before January 1...) and tax on the sale of gasoline, diesel fuel or other motor fuel paid by the consumer (other than in...

26 CFR 1.164-5 - Certain retail sales taxes and gasoline taxes.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 2 2010-04-01 2010-04-01 false Certain retail sales taxes and gasoline taxes. 1....164-5 Certain retail sales taxes and gasoline taxes. For taxable years beginning before January 1...) and tax on the sale of gasoline, diesel fuel or other motor fuel paid by the consumer (other than in...

26 CFR 1.164-5 - Certain retail sales taxes and gasoline taxes.

Code of Federal Regulations, 2014 CFR

2014-04-01

... 26 Internal Revenue 2 2014-04-01 2014-04-01 false Certain retail sales taxes and gasoline taxes. 1....164-5 Certain retail sales taxes and gasoline taxes. For taxable years beginning before January 1...) and tax on the sale of gasoline, diesel fuel or other motor fuel paid by the consumer (other than in...

A Critical Role for IL-17RB Signaling in HTLV-1 Tax-Induced NF-κB Activation and T-Cell Transformation

PubMed Central

Lavorgna, Alfonso; Matsuoka, Masao; Harhaj, Edward William

2014-01-01

Human T-cell leukemia virus type 1 (HTLV-1) infection is linked to the development of adult T-cell leukemia (ATL) and the neuroinflammatory disease HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax protein functions as a potent viral oncogene that constitutively activates the NF-κB transcription factor to transform T cells; however, the underlying mechanisms remain obscure. Here, using next-generation RNA sequencing we identified the IL-25 receptor subunit IL-17RB as an aberrantly overexpressed gene in HTLV-1 immortalized T cells. Tax induced the expression of IL-17RB in an IκB kinase (IKK) and NF-κB-dependent manner. Remarkably, Tax activation of the canonical NF-κB pathway in T cells was critically dependent on IL-17RB expression. IL-17RB and IL-25 were required for HTLV-1-induced immortalization of primary T cells, and the constitutive NF-κB activation and survival of HTLV-1 transformed T cells. IL-9 was identified as an important downstream target gene of the IL-17RB pathway that drives the proliferation of HTLV-1 transformed cells. Furthermore, IL-17RB was overexpressed in leukemic cells from a subset of ATL patients and also regulated NF-κB activation in some, but not all, Tax-negative ATL cell lines. Together, our results support a model whereby Tax instigates an IL-17RB-NF-κB feed-forward autocrine loop that is obligatory for HTLV-1 leukemogenesis. PMID:25340344

26 CFR 301.6316-5 - Manner of paying tax by foreign currency.

Code of Federal Regulations, 2010 CFR

2010-04-01

... currency to be deposited shall be that amount which, when converted at the rate of exchange used on the... 26 Internal Revenue 18 2010-04-01 2010-04-01 false Manner of paying tax by foreign currency. 301....6316-5 Manner of paying tax by foreign currency. (a) Time and place to pay. The unpaid tax required to...

At-TAX: a whole genome tiling array resource for developmental expression analysis and transcript identification in Arabidopsis thaliana

PubMed Central

Laubinger, Sascha; Zeller, Georg; Henz, Stefan R; Sachsenberg, Timo; Widmer, Christian K; Naouar, Naïra; Vuylsteke, Marnik; Schölkopf, Bernhard; Rätsch, Gunnar; Weigel, Detlef

2008-01-01

Gene expression maps for model organisms, including Arabidopsis thaliana, have typically been created using gene-centric expression arrays. Here, we describe a comprehensive expression atlas, Arabidopsis thaliana Tiling Array Express (At-TAX), which is based on whole-genome tiling arrays. We demonstrate that tiling arrays are accurate tools for gene expression analysis and identified more than 1,000 unannotated transcribed regions. Visualizations of gene expression estimates, transcribed regions, and tiling probe measurements are accessible online at the At-TAX homepage. PMID:18613972

Bromodomain and Extraterminal (BET) Protein Inhibition Suppresses Human T Cell Leukemia Virus 1 (HTLV-1) Tax Protein-mediated Tumorigenesis by Inhibiting Nuclear Factor κB (NF-κB) Signaling*

PubMed Central

Wu, Xuewei; Qi, Jun; Bradner, James E.; Xiao, Gutian; Chen, Lin-Feng

2013-01-01

The etiology of human T cell leukemia virus 1 (HTLV-1)-mediated adult T cell leukemia is associated with the ability of viral oncoprotein Tax to induce sustained NF-κB activation and the expression of many NF-κB target genes. Acetylation of the RelA subunit of NF-κB and the subsequent recruitment of bromodomain-containing factor Brd4 are important for the expression of NF-κB target genes in response to various stimuli. However, their contributions to Tax-mediated NF-κB target gene expression and tumorigenesis remain unclear. Here we report that Tax induced the acetylation of lysine 310 of RelA and the binding of Brd4 to acetylated RelA to facilitate Tax-mediated transcriptional activation of NF-κB. Depletion of Brd4 down-regulated Tax-mediated NF-κB target gene expression and cell proliferation. Inhibiting the interaction of Brd4 and acetylated RelA with the bromodomain extraterminal protein inhibitor JQ1 suppressed the proliferation of Tax-expressing rat fibroblasts and Tax-positive HTLV-1-infected cells and Tax-mediated cell transformation and tumorigenesis. Moreover, JQ1 attenuated the Tax-mediated transcriptional activation of NF-κB, triggering the polyubiquitination and proteasome-mediated degradation of constitutively active nuclear RelA. Our results identify Brd4 as a key regulator for Tax-mediated NF-κB gene expression and suggest that targeting epigenetic regulators such as Brd4 with the bromodomain extraterminal protein inhibitor might be a potential therapeutic strategy for cancers and other diseases associated with HTLV-1 infection. PMID:24189064

Evidence that Mediator is essential for Pol II transcription, but is not a required component of the preinitiation complex in vivo.

PubMed

Petrenko, Natalia; Jin, Yi; Wong, Koon Ho; Struhl, Kevin

2017-07-12

The Mediator complex has been described as a general transcription factor, but it is unclear if it is essential for Pol II transcription and/or is a required component of the preinitiation complex (PIC) in vivo. Here, we show that depletion of individual subunits, even those essential for cell growth, causes a general but only modest decrease in transcription. In contrast, simultaneous depletion of all Mediator modules causes a drastic decrease in transcription. Depletion of head or middle subunits, but not tail subunits, causes a downstream shift in the Pol II occupancy profile, suggesting that Mediator at the core promoter inhibits promoter escape. Interestingly, a functional PIC and Pol II transcription can occur when Mediator is not detected at core promoters. These results provide strong evidence that Mediator is essential for Pol II transcription and stimulates PIC formation, but it is not a required component of the PIC in vivo.

Implications of new accounting rules for income taxes.

PubMed

Reinstein, A; Carmichael, B J; Spaulding, A D

1994-02-01

The provisions of the Financial Accounting Standards Board (FASB) Statement No. 109, Accounting for Income Taxes, require all organizations that issue financial statements to shift the focus of their accounting for income taxes from the income statement to the balance sheet. This change can alter significantly a healthcare organization's financial position. The change also may affect the way in which investors, lenders, regulators, and other users of financial statements evaluate corporations in the healthcare industry. Hospitals and other healthcare organizations, particularly for-profit organizations, therefore, should review carefully their methods of accounting for such items as deferred tax assets and loss and expense reserves.

Tax subsidization of personal assistance services.

PubMed

Mendelsohn, Steven; Myhill, William N; Morris, Michael

2012-04-01

Personal assistance services (PAS) is the term used to describe the range of assistance, services, and supports many people with disabilities and older Americans need to remain in their homes and communities. The Americans with Disabilities Act requires that people with disabilities receive essential services in the communities of their choice rather than in institutional settings. PAS availability often determines whether persons with disabilities become institutionalized or remain in their communities. PAS, however, are not inexpensive or broadly available. Strategies are needed to improve their availability to people with disabilities and the elderly. We sought to analyze 8 provisions of the Internal Revenue Code for their utility to make PAS more affordable and available. The authors conducted a legal analysis of 8 statutory provisions, as interpreted by regulations, court decisions, and other authoritative sources. Each of the tax provisions analyzed covers some PAS expenses incurred by an individual or family. Favorable tax treatment is impacted by the nature and amount of expenses and by the location and conditions of services. The current limitations and complexities of legal interpretations and the fact that many individuals with disabilities are uninformed about these tax provisions present challenges and opportunities. As the need for PAS grows, reform of tax policy is an important complement to health care and long-term services and supports for people with disabilities. To increase utilization of current beneficial tax provisions that subsidize the cost of PAS, individuals with disabilities and tax preparers must become better informed about using these provisions. Copyright © 2012 Elsevier Inc. All rights reserved.

Income Tax Law: U.S. Armed Forces Training: Course Book.

ERIC Educational Resources Information Center

Internal Revenue Service (Dept. of Treasury), Washington, DC.

The course book contains eight lessons designed for military Personnel learning how to properly prepare their U.S. Income Tax returns. The lessons cover the following subjects: requirments for filing returns of income and declaration of estimated tax; exemptions; gross income; exclusions and deductions to arrive at adjusted gross income;…

Income Tax Law: U.S. Armed Forces Training: Instructor Guide.

ERIC Educational Resources Information Center

Internal Revenue Service (Dept. of Treasury), Washington, DC.

The instructor's guide provides eight detailed lesson plans for instructing military personnel in the preparation of their U.S. Income Tax Returns. The plans cover the following subjects: requirements for filing returns of income and declaration of estimated tax; exemptions; gross income; exclusions and deductions to arrive at adjusted gross…

78 FR 71039 - Publication of the Tier 2 Tax Rates

Federal Register 2010, 2011, 2012, 2013, 2014

2013-11-27

...Publication of the tier 2 tax rates for calendar year 2014 as required by section 3241(d) of the Internal Revenue Code (26 U.S.C. section 3241). Tier 2 taxes on railroad employees, employers, and employee representatives are one source of funding for benefits under the Railroad Retirement Act.

Women and Tax Policy.

ERIC Educational Resources Information Center

Ruttenberg, Ruth; McCarthy, Amy

The major types of U.S. federal, state, and local taxes are explored, and the impact of those taxes on all types of women--rich and poor, old and young, employed and not employed, parent and non-parent--are examined. Specifically discussed are the social security tax; the federal income tax system, including the marriage tax, the earned income…

Evidence that Mediator is essential for Pol II transcription, but is not a required component of the preinitiation complex in vivo

PubMed Central

Petrenko, Natalia; Jin, Yi; Wong, Koon Ho; Struhl, Kevin

2017-01-01

The Mediator complex has been described as a general transcription factor, but it is unclear if it is essential for Pol II transcription and/or is a required component of the preinitiation complex (PIC) in vivo. Here, we show that depletion of individual subunits, even those essential for cell growth, causes a general but only modest decrease in transcription. In contrast, simultaneous depletion of all Mediator modules causes a drastic decrease in transcription. Depletion of head or middle subunits, but not tail subunits, causes a downstream shift in the Pol II occupancy profile, suggesting that Mediator at the core promoter inhibits promoter escape. Interestingly, a functional PIC and Pol II transcription can occur when Mediator is not detected at core promoters. These results provide strong evidence that Mediator is essential for Pol II transcription and stimulates PIC formation, but it is not a required component of the PIC in vivo. DOI: http://dx.doi.org/10.7554/eLife.28447.001 PMID:28699889

Chromatin Redistribution of the DEK Oncoprotein Represses hTERT Transcription in Leukemias12

PubMed Central

Karam, Maroun; Thenoz, Morgan; Capraro, Valérie; Robin, Jean-Philippe; Pinatel, Christiane; Lancon, Agnès; Galia, Perrine; Sibon, David; Thomas, Xavier; Ducastelle-Lepretre, Sophie; Nicolini, Franck; El-Hamri, Mohamed; Chelghoun, Youcef; Wattel, Eric; Mortreux, Franck

2014-01-01

Although numerous factors have been found to modulate hTERT transcription, the mechanism of its repression in certain leukemias remains unknown. We show here that DEK represses hTERT transcription through its enrichment on the hTERT promoter in cells from chronic and acute myeloid leukemias, chronic lymphocytic leukemia, but not acute lymphocytic leukemias where hTERT is overexpressed. We isolated DEK from the hTERT promoter incubated with nuclear extracts derived from fresh acute myelogenous leukemia (AML) cells and from cells expressing Tax, an hTERT repressor encoded by the human T cell leukemia virus type 1. In addition to the recruitment of DEK, the displacement of two potent known hTERT transactivators from the hTERT promoter characterized both AML cells and Tax-expressing cells. Reporter and chromatin immunoprecipitation assays permitted to map the region that supports the repressive effect of DEK on hTERT transcription, which was proportionate to the level of DEK-promoter association but not with the level of DEK expression. Besides hTERT repression, this context of chromatin redistribution of DEK was found to govern about 40% of overall transcriptional modifications, including those of cancer-prone genes. In conclusion, DEK emerges as an hTERT repressor shared by various leukemia subtypes and seems involved in the deregulation of numerous genes associated with leukemogenesis. PMID:24563617

Commensal Microbiota Contributes to Chronic Endocarditis in TAX1BP1 Deficient Mice

PubMed Central

Nakano, Satoko; Ikebe, Emi; Tsukamoto, Yoshiyuki; Wang, Yan; Matsumoto, Takashi; Mitsui, Takahiro; Yahiro, Takaaki; Inoue, Kunimitsu; Kawazato, Hiroaki; Yasuda, Aiko; Ito, Kanako; Yokoyama, Shigeo; Takahashi, Naohiko; Hori, Mitsuo; Shimada, Tatsuo; Moriyama, Masatsugu; Kubota, Toshiaki; Ono, Katsushige; Fujibuchi, Wataru; Jeang, Kuan-Teh; Iha, Hidekatsu; Nishizono, Akira

2013-01-01

Tax1-binding protein 1 (Tax1bp1) negatively regulates NF-κB by editing the ubiquitylation of target molecules by its catalytic partner A20. Genetically engineered TAX1BP1-deficient (KO) mice develop age-dependent inflammatory constitutions in multiple organs manifested as valvulitis or dermatitis and succumb to premature death. Laser capture dissection and gene expression microarray analysis on the mitral valves of TAX1BP1-KO mice (8 and 16 week old) revealed 588 gene transcription alterations from the wild type. SAA3 (serum amyloid A3), CHI3L1, HP, IL1B and SPP1/OPN were induced 1,180-, 361-, 187-, 122- and 101-fold respectively. WIF1 (Wnt inhibitory factor 1) exhibited 11-fold reduction. Intense Saa3 staining and significant I-κBα reduction were reconfirmed and massive infiltration of inflammatory lymphocytes and edema formation were seen in the area. Antibiotics-induced ‘germ free’ status or the additional MyD88 deficiency significantly ameliorated TAX1BP1-KO mice's inflammatory lesions. These pathological conditions, as we named ‘pseudo-infective endocarditis’ were boosted by the commensal microbiota who are usually harmless by their nature. This experimental outcome raises a novel mechanistic linkage between endothelial inflammation caused by the ubiquitin remodeling immune regulators and fatal cardiac dysfunction. PMID:24086273

Updated Tax Tips for Forest Landowners for the 2010 Tax Year

Treesearch

Linda Wang; John L. Greene

2010-01-01

This bulletin is updated as of Dec. 20, 2010, to include the changes from Public Law 111-31 enacted on Dec. 17, 2010. It provides tax tips for woodland owners and their tax advisors in the preparation of the 2010 individual tax return. Please be aware the information presented here is not legal or accounting advice. Consult your legal and tax advisors for more complete...

Enhancing Tax Compliance through Coercive and Legitimate Power of Tax Authorities by Concurrently Diminishing or Facilitating Trust in Tax Authorities.

PubMed

Hofmann, Eva; Gangl, Katharina; Kirchler, Erich; Stark, Jennifer

2014-07-01

Both coercion, such as strict auditing and the use of fines, and legitimate procedures, such as assistance by tax authorities, are often discussed as means of enhancing tax compliance. However, the psychological mechanisms that determine the effectiveness of each strategy are not clear. Although highly relevant, there is rare empirical literature examining the effects of both strategies applied in combination. It is assumed that coercion decreases implicit trust in tax authorities, leading to the perception of a hostile antagonistic tax climate and enforced tax compliance. Conversely, it is suggested that legitimate power increases reason-based trust in the tax authorities, leading to the perception of a service climate and eventually to voluntary cooperation. The combination of both strategies is assumed to cause greater levels of intended compliance than each strategy alone. We conducted two experimental studies with convenience samples of 261 taxpayers overall. The studies describe tax authorities as having low or high coercive power (e.g., imposing lenient or severe sanctions) and/or low or high legitimate power (e.g., having nontransparent or transparent procedures). Data analyses provide supportive evidence for the assumptions regarding the impact on intended tax compliance. Coercive power did not reduce implicit trust in tax authorities; however, it had an effect on reason-based trust, interaction climate, and intended tax compliance if applied solely. When wielded in combination with legitimate power, it had no effect.

26 CFR 1.6017-1 - Self-employment tax returns.

Code of Federal Regulations, 2010 CFR

2010-04-01

... Revenue Service to such resident for use in lieu of Form 1040SS. (b) Joint returns. (1) In the case of a.... The requirement of section 6013(d)(3) that in the case of a joint return the tax is computed on the... tax in the case of a joint return is joint and several. (c) Social security account numbers. (1) Every...

Tax Tips for Forest Landowners for the 2007 Tax Year

Treesearch

Linda Wang; John L. Greene

2007-01-01

This guide is designed to assist owners of forest land with timber tax information. It is current as of October 1, 2007, and supercedes Management Bulletin R8-MB 128. It is strictly for educational purposes; consult your legal and tax professionals for advice on a specific tax situation.

Undermining government tax policies: Common legal strategies employed by the tobacco industry in response to tobacco tax increases.

PubMed

Ross, H; Tesche, J; Vellios, N

2017-12-01

Effective tobacco tax increases reduce tobacco consumption, threatening the profitability of the tobacco industry. In response, the tobacco industry employs strategies to negate or minimize the full effects of tobacco tax increases. By interacting with various government agencies and non-governmental organizations we identified seven such strategies: stockpiling, changing product attributes or production processes, lowering prices, over-shifting prices, under-shifting prices, timing of price increases, and engaging in price discrimination and/or offering promotions. Each strategy is described in terms of the motivation for their employment, the consequences for tobacco use and tax revenue, and measures to counter them. Country case studies illustrate the successful execution of the strategies and possible government responses. Many of the tobacco industry's responses to tobacco tax increases are predictable, since they are being employed systematically across countries. Governments can and should adopt appropriate measures to eliminate or reduce tobacco industry manipulation. This requires systematic data collection in order to monitor tobacco industry behavior. Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

Precise assignment of the heavy-strand promoter of mouse mitochondrial DNA: cognate start sites are not required for transcriptional initiation.

PubMed Central

Chang, D D; Clayton, D A

1986-01-01

Transcription of the heavy strand of mouse mitochondrial DNA starts from two closely spaced, distinct sites located in the displacement loop region of the genome. We report here an analysis of regulatory sequences required for faithful transcription from these two sites. Data obtained from in vitro assays demonstrated that a 51-base-pair region, encompassing nucleotides -40 to +11 of the downstream start site, contains sufficient information for accurate transcription from both start sites. Deletion of the 3' flanking sequences, including one or both start sites to -17, resulted in the initiation of transcription by the mitochondrial RNA polymerase from alternative sites within vector DNA sequences. This feature places the mouse heavy-strand promoter uniquely among other known mitochondrial promoters, all of which absolutely require cognate start sites for transcription. Comparison of the heavy-strand promoter with those of other vertebrate mitochondrial DNAs revealed a remarkably high rate of sequence divergence among species. Images PMID:3785226

Cigarette tax avoidance and evasion.

PubMed

Stehr, Mark

2005-03-01

Variation in state cigarette taxes provides incentives for tax avoidance through smuggling, legal border crossing to low tax jurisdictions, or Internet purchasing. When taxes rise, tax paid sales of cigarettes will decline both because consumption will decrease and because tax avoidance will increase. The key innovation of this paper is to compare cigarette sales data to cigarette consumption data from the Behavioral Risk Factor Surveillance System (BRFSS). I show that after subtracting percent changes in consumption, residual percent changes in sales are associated with state cigarette tax changes implying the existence of tax avoidance. I estimate that the tax avoidance response to tax changes is at least twice the consumption response and that tax avoidance accounted for up to 9.6% of sales between 1985 and 2001. Because of the increase in tax avoidance, tax paid sales data understate the level of smoking and overstate the drop in smoking. I also find that the level of legal border crossing was very low relative to other forms of tax avoidance. If states have strong preferences for smoking control, they must pair high cigarette taxes with effective policies to curb smuggling and other forms of tax avoidance or employ alternative policies such as counter-advertising and smoking restrictions.

Human T-lymphotropic Virus Type 1-infected Cells Secrete Exosomes That Contain Tax Protein*

PubMed Central

Jaworski, Elizabeth; Narayanan, Aarthi; Van Duyne, Rachel; Shabbeer-Meyering, Shabana; Iordanskiy, Sergey; Saifuddin, Mohammed; Das, Ravi; Afonso, Philippe V.; Sampey, Gavin C.; Chung, Myung; Popratiloff, Anastas; Shrestha, Bindesh; Sehgal, Mohit; Jain, Pooja; Vertes, Akos; Mahieux, Renaud; Kashanchi, Fatah

2014-01-01

Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis. The HTLV-1 transactivator protein Tax controls many critical cellular pathways, including host cell DNA damage response mechanisms, cell cycle progression, and apoptosis. Extracellular vesicles called exosomes play critical roles during pathogenic viral infections as delivery vehicles for host and viral components, including proteins, mRNA, and microRNA. We hypothesized that exosomes derived from HTLV-1-infected cells contain unique host and viral proteins that may contribute to HTLV-1-induced pathogenesis. We found exosomes derived from infected cells to contain Tax protein and proinflammatory mediators as well as viral mRNA transcripts, including Tax, HBZ, and Env. Furthermore, we observed that exosomes released from HTLV-1-infected Tax-expressing cells contributed to enhanced survival of exosome-recipient cells when treated with Fas antibody. This survival was cFLIP-dependent, with Tax showing induction of NF-κB in exosome-recipient cells. Finally, IL-2-dependent CTLL-2 cells that received Tax-containing exosomes were protected from apoptosis through activation of AKT. Similar experiments with primary cultures showed protection and survival of peripheral blood mononuclear cells even in the absence of phytohemagglutinin/IL-2. Surviving cells contained more phosphorylated Rb, consistent with the role of Tax in regulation of the cell cycle. Collectively, these results suggest that exosomes may play an important role in extracellular delivery of functional HTLV-1 proteins and mRNA to recipient cells. PMID:24939845

Cigarette Taxes and Smoking Participation: Evidence from Recent Tax Increases in Canada

PubMed Central

Azagba, Sunday; Sharaf, Mesbah

2011-01-01

Using the Canadian National Population Health Survey and the recent tax variation across Canadian provinces, this paper examines the impact of cigarette taxes on smoking participation. Consistent with the literature, we find evidence of a heterogeneous response to cigarette taxes among different groups of smokers. Contrary to most studies, we find that the middle age group—which constitutes the largest fraction of smokers in our sample—is largely unresponsive to taxes. While cigarette taxes remain popular with policy makers as an anti-smoking measure, identifying the socio-demographic characteristics of smokers who respond differentially to tax increase will help in designing appropriate supplementary measures to reduce smoking. PMID:21655139

26 CFR 1.312-8 - Effect on earnings and profits of receipt of tax-free distributions requiring adjustment or...

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 4 2011-04-01 2011-04-01 false Effect on earnings and profits of receipt of tax...) INCOME TAXES Effects on Corporation § 1.312-8 Effect on earnings and profits of receipt of tax-free... earnings and profits, where a corporation receives (after February 28, 1913) from a second corporation a...

26 CFR 1.312-8 - Effect on earnings and profits of receipt of tax-free distributions requiring adjustment or...

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 4 2010-04-01 2010-04-01 false Effect on earnings and profits of receipt of tax...) INCOME TAXES Effects on Corporation § 1.312-8 Effect on earnings and profits of receipt of tax-free... earnings and profits, where a corporation receives (after February 28, 1913) from a second corporation a...

Enhancing Tax Compliance through Coercive and Legitimate Power of Tax Authorities by Concurrently Diminishing or Facilitating Trust in Tax Authorities

PubMed Central

Hofmann, Eva; Gangl, Katharina; Kirchler, Erich; Stark, Jennifer

2014-01-01

Both coercion, such as strict auditing and the use of fines, and legitimate procedures, such as assistance by tax authorities, are often discussed as means of enhancing tax compliance. However, the psychological mechanisms that determine the effectiveness of each strategy are not clear. Although highly relevant, there is rare empirical literature examining the effects of both strategies applied in combination. It is assumed that coercion decreases implicit trust in tax authorities, leading to the perception of a hostile antagonistic tax climate and enforced tax compliance. Conversely, it is suggested that legitimate power increases reason-based trust in the tax authorities, leading to the perception of a service climate and eventually to voluntary cooperation. The combination of both strategies is assumed to cause greater levels of intended compliance than each strategy alone. We conducted two experimental studies with convenience samples of 261 taxpayers overall. The studies describe tax authorities as having low or high coercive power (e.g., imposing lenient or severe sanctions) and/or low or high legitimate power (e.g., having nontransparent or transparent procedures). Data analyses provide supportive evidence for the assumptions regarding the impact on intended tax compliance. Coercive power did not reduce implicit trust in tax authorities; however, it had an effect on reason-based trust, interaction climate, and intended tax compliance if applied solely. When wielded in combination with legitimate power, it had no effect. PMID:26074656

HTLV-1 Tax-mediated inhibition of FOXO3a activity is critical for the persistence of terminally differentiated CD4+ T cells.

PubMed

Olagnier, David; Sze, Alexandre; Bel Hadj, Samar; Chiang, Cindy; Steel, Courtney; Han, Xiaoying; Routy, Jean-Pierre; Lin, Rongtuan; Hiscott, John; van Grevenynghe, Julien

2014-12-01

The mechanisms involved in the persistence of activated CD4+ T lymphocytes following primary human T leukemia/lymphoma virus type 1 (HTLV-1) infection remain unclear. Here, we demonstrate that the HTLV-1 Tax oncoprotein modulates phosphorylation and transcriptional activity of the FOXO3a transcription factor, via upstream activation of the AKT pathway. De novo HTLV-1 infection of CD4+ T cells or direct lentiviral-mediated introduction of Tax led to AKT activation and AKT-dependent inactivation of FOXO3a, via phosphorylation of residues Ser253 and Thr32. Inhibition of FOXO3a signalling led to the long-term survival of a population of highly activated, terminally differentiated CD4+Tax+CD27negCCR7neg T cells that maintained the capacity to disseminate infectious HTLV-1. CD4+ T cell persistence was reversed by chemical inhibition of AKT activity, lentiviral-mediated expression of a dominant-negative form of FOXO3a or by specific small interfering RNA (siRNA)-mediated silencing of FOXO3a. Overall this study provides new mechanistic insight into the strategies used by HTLV-1 to increase long-term maintenance of Tax+CD4+ T lymphocytes during the early stages of HTLV-1 pathogenesis.

HTLV-1 Tax-Mediated Inhibition of FOXO3a Activity Is Critical for the Persistence of Terminally Differentiated CD4+ T Cells

PubMed Central

Bel Hadj, Samar; Chiang, Cindy; Steel, Courtney; Han, Xiaoying; Routy, Jean-Pierre; Lin, Rongtuan; Hiscott, John; van Grevenynghe, Julien

2014-01-01

The mechanisms involved in the persistence of activated CD4+ T lymphocytes following primary human T leukemia/lymphoma virus type 1 (HTLV-1) infection remain unclear. Here, we demonstrate that the HTLV-1 Tax oncoprotein modulates phosphorylation and transcriptional activity of the FOXO3a transcription factor, via upstream activation of the AKT pathway. De novo HTLV-1 infection of CD4+ T cells or direct lentiviral-mediated introduction of Tax led to AKT activation and AKT-dependent inactivation of FOXO3a, via phosphorylation of residues Ser253 and Thr32. Inhibition of FOXO3a signalling led to the long-term survival of a population of highly activated, terminally differentiated CD4+Tax+CD27negCCR7neg T cells that maintained the capacity to disseminate infectious HTLV-1. CD4+ T cell persistence was reversed by chemical inhibition of AKT activity, lentiviral-mediated expression of a dominant-negative form of FOXO3a or by specific small interfering RNA (siRNA)-mediated silencing of FOXO3a. Overall this study provides new mechanistic insight into the strategies used by HTLV-1 to increase long-term maintenance of Tax+CD4+ T lymphocytes during the early stages of HTLV-1 pathogenesis. PMID:25521510

Taxes and You. 1999 Edition. An Educational Curriculum on Federal Income Tax.

ERIC Educational Resources Information Center

Internal Revenue Service (Dept. of Treasury), Washington, DC.

This comprehensive educational curriculum aims to teach adults about federal income taxes and the role of taxes in the economy. The unit provides the tools, lessons, and activities to teach information about taxes and tax forms. The lessons build upon each other. Two instructional modules can be used separately as workshop topics, integrated into…

Tax Tips for Forest Landowners for the 2012 Tax Year

Treesearch

Linda Wang; John L. Greene

2012-01-01

Federal income tax law contains provisions to encourage stewardship and management of private forest land. The primary goal of this bulletin is to assist forest landowners and their advisors with timber tax information they can use to file their 2012 in-come tax returns. The information presented here is current as of Sept. 15, 2012.

Role of Tax protein in human T-cell leukemia virus type-I leukemogenicity

PubMed Central

Azran, Inbal; Schavinsky-Khrapunsky, Yana; Aboud, Mordechai

2004-01-01

HTLV-1 is the etiological agent of adult T-cell leukemia (ATL), the neurological syndrome TSP/HAM and certain other clinical disorders. The viral Tax protein is considered to play a central role in the process leading to ATL. Tax modulates the expression of many viral and cellular genes through the CREB/ATF-, SRF- and NF-κB-associated pathways. In addition, Tax employs the CBP/p300 and p/CAF co-activators for implementing the full transcriptional activation competence of each of these pathways. Tax also affects the function of various other regulatory proteins by direct protein-protein interaction. Through these activities Tax sets the infected T-cells into continuous uncontrolled replication and destabilizes their genome by interfering with the function of telomerase and topoisomerase-I and by inhibiting DNA repair. Furthermore, Tax prevents cell cycle arrest and apoptosis that would otherwise be induced by the unrepaired DNA damage and enables, thereby, accumulation of mutations that can contribute to the leukemogenic process. Together, these capacities render Tax highly oncogenic as reflected by its ability to transform rodent fibroblasts and primary human T-cells and to induce tumors in transgenic mice. In this article we discuss these effects of Tax and their apparent contribution to the HTLV-1 associated leukemogenic process. Notably, however, shortly after infection the virus enters into a latent state, in which viral gene expression is low in most of the HTLV-1 carriers' infected T-cells and so is the level of Tax protein, although rare infected cells may still display high viral RNA. This low Tax level is evidently insufficient for exerting its multiple oncogenic effects. Therefore, we propose that the latent virus must be activated, at least temporarily, in order to elevate Tax to its effective level and that during this transient activation state the infected cells may acquire some oncogenic mutations which can enable them to further progress towards

Role of Tax protein in human T-cell leukemia virus type-I leukemogenicity.

PubMed

Azran, Inbal; Schavinsky-Khrapunsky, Yana; Aboud, Mordechai

2004-08-13

HTLV-1 is the etiological agent of adult T-cell leukemia (ATL), the neurological syndrome TSP/HAM and certain other clinical disorders. The viral Tax protein is considered to play a central role in the process leading to ATL. Tax modulates the expression of many viral and cellular genes through the CREB/ATF-, SRF- and NF-kappaB-associated pathways. In addition, Tax employs the CBP/p300 and p/CAF co-activators for implementing the full transcriptional activation competence of each of these pathways. Tax also affects the function of various other regulatory proteins by direct protein-protein interaction. Through these activities Tax sets the infected T-cells into continuous uncontrolled replication and destabilizes their genome by interfering with the function of telomerase and topoisomerase-I and by inhibiting DNA repair. Furthermore, Tax prevents cell cycle arrest and apoptosis that would otherwise be induced by the unrepaired DNA damage and enables, thereby, accumulation of mutations that can contribute to the leukemogenic process. Together, these capacities render Tax highly oncogenic as reflected by its ability to transform rodent fibroblasts and primary human T-cells and to induce tumors in transgenic mice. In this article we discuss these effects of Tax and their apparent contribution to the HTLV-1 associated leukemogenic process. Notably, however, shortly after infection the virus enters into a latent state, in which viral gene expression is low in most of the HTLV-1 carriers' infected T-cells and so is the level of Tax protein, although rare infected cells may still display high viral RNA. This low Tax level is evidently insufficient for exerting its multiple oncogenic effects. Therefore, we propose that the latent virus must be activated, at least temporarily, in order to elevate Tax to its effective level and that during this transient activation state the infected cells may acquire some oncogenic mutations which can enable them to further progress towards

Taxing junk food: applying the logic of the Henry tax review to food.

PubMed

Bond, Molly E; Williams, Michael J; Crammond, Brad; Loff, Bebe

2010-10-18

The recent review of taxation in Australia - the Henry tax review - has recommended that the federal government increase the taxes already levied on tobacco and alcohol. Tobacco and alcohol taxes are put forward as the best way of reducing the social harms caused by the use and misuse of these substances. Junk foods have the same pattern of misuse and the same social costs as tobacco and alcohol. The Henry tax review rejects the idea of taxing fatty foods, and to date the government has not implemented a tax on junk food. We propose that a tax on junk food be implemented as a tool to reduce consumption and address the obesity epidemic.

Transcript of the Joint FAA/Industry Symposium on Level B Airplane simulator aeromodel validation requirements

DOT National Transportation Integrated Search

1996-03-13

"This is the transcript of the Joint FAA/Industry Symposium on Level B Airplane Simulator Aeromodel Validation Requirements held on March 13-14, 1996, at the Washington Dulles Airport Hilton. The purpose of the meeting was to discuss the aeromodeling...

The Tax Compliance Demand Curve: A Diagrammatical Approach to Income Tax Evasion

ERIC Educational Resources Information Center

Yaniv, Gideon

2009-01-01

One of the most interesting results in the tax evasion literature is that an increase in the income tax rate would increase tax compliance. Despite its peculiarity, this result has gained acceptance as a cornerstone for further developments of the rational tax evasion model. However, because of the mathematical format by which it is conveyed, this…

75 FR 9141 - Reduced 2009 Estimated Income Tax Payments for Individuals With Small Business Income

Federal Register 2010, 2011, 2012, 2013, 2014

2010-03-01

... Reduced 2009 Estimated Income Tax Payments for Individuals With Small Business Income AGENCY: Internal... their required 2009 estimated income tax payments. The temporary regulations implement section 1212 of... Revenue Code (Code) to provide for reduced 2009 estimated income tax payments for certain qualified...

48 CFR 1632.607 - Tax credit.

Code of Federal Regulations, 2012 CFR

2012-10-01

... 48 Federal Acquisition Regulations System 6 2012-10-01 2012-10-01 false Tax credit. 1632.607 Section 1632.607 Federal Acquisition Regulations System OFFICE OF PERSONNEL MANAGEMENT FEDERAL EMPLOYEES HEALTH BENEFITS ACQUISITION REGULATION GENERAL CONTRACTING REQUIREMENTS CONTRACT FINANCING Contract Debts...

48 CFR 1632.607 - Tax credit.

Code of Federal Regulations, 2014 CFR

2014-10-01

... 48 Federal Acquisition Regulations System 6 2014-10-01 2014-10-01 false Tax credit. 1632.607 Section 1632.607 Federal Acquisition Regulations System OFFICE OF PERSONNEL MANAGEMENT FEDERAL EMPLOYEES HEALTH BENEFITS ACQUISITION REGULATION GENERAL CONTRACTING REQUIREMENTS CONTRACT FINANCING Contract Debts...

Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product.

PubMed

Parra, Eduardo; Gutierréz, Luís; Ferreira, Jorge

2016-02-01

The Tax protein of human T cell leukemia virus type 1 plays a major role in the pathogenesis of adult T cell leukemia (ATL), an aggressive neoplasia of CD4+ T cells. In the present study, we investigated whether the EGR-1 pathway is involved in the regulation of Tax-induced JNK expression in human Jurkat T cells transfected to express the Tax protein in the presence or absence of PMA or ionomycin. Overexpression of EGR-1 in Jurkat cells transfected to express Tax, promoted the activation of several genes, with the most potent being those that contained AP-1 (Jun/c-Fos), whereas knockdown of endogenous EGR-1 by small interfering RNA (siRNA) somewhat reduced Tax-mediated JNK-1 transcription. Additionally, luciferase-based AP-1 and NF-κB reporter gene assays demonstrated that inhibition of EGR-1 expression by an siRNA did not affect the transcriptional activity of a consensus sequence of either AP-1 or NF-κB. On the other hand, the apoptosis assay, using all-trans retinoic acid (ATRA) as an inducer of apoptosis, confirmed that siRNA against EGR-1 failed to suppress ATRA-induced apoptosis in Jurkat and Jurkat-Tax cells, as noted by the low levels of both DEVDase activity and DNA fragmentation, indicating that the induction of apoptosis by ATRA was Egr-1-independent. Finally, our data showed that activation of Tax by JNK-1 was not dependent on the EGR-1 cascade of events, suggesting that EGR-1 is important but not a determinant for the activity for Tax-induced proliferation of Jurkat cells.

Rich and Well Educated: Are These Requirements Necessary to Claim Healthcare Tax Credits in Italy?

PubMed

Brenna, Elenka

2018-04-01

The paper investigates the use of healthcare tax credits (HTCs) in Italy through the analysis of a panel data, which provides information on individual income tax from 2008 to 2014. There is evidence of disparities in the per-capita HTCs between Northern and Southern regions, which need to be analyzed and addressed. The aim of the paper is to investigate the socioeconomic determinants in the use of Healthcare Tax Credits in Italy. A fixed effects Ordinary Least Square model is run to analyze the impact of selected socioeconomic variables on regional per capita HTCs, with a particular focus on the role of education. The results corroborate literature findings on the regressive effects of HTCs; they also provide highlights on the role of education in explaining the distribution of HTCs among Italian regions. Public money is reimbursed to regions where people are, on average, richer and better educated. More equitable objectives could be reached by allocating the same resources in the provision of services covered by the NHS.

Timing of Tissue-specific Cell Division Requires a Differential Onset of Zygotic Transcription during Metazoan Embryogenesis*

PubMed Central

Wong, Ming-Kin; Guan, Daogang; Ng, Kaoru Hon Chun; Ho, Vincy Wing Sze; An, Xiaomeng; Li, Runsheng; Ren, Xiaoliang

2016-01-01

Metazoan development demands not only precise cell fate differentiation but also accurate timing of cell division to ensure proper development. How cell divisions are temporally coordinated during development is poorly understood. Caenorhabditis elegans embryogenesis provides an excellent opportunity to study this coordination due to its invariant development and widespread division asynchronies. One of the most pronounced asynchronies is a significant delay of cell division in two endoderm progenitor cells, Ea and Ep, hereafter referred to as E2, relative to its cousins that mainly develop into mesoderm organs and tissues. To unravel the genetic control over the endoderm-specific E2 division timing, a total of 822 essential and conserved genes were knocked down using RNAi followed by quantification of cell cycle lengths using in toto imaging of C. elegans embryogenesis and automated lineage. Intriguingly, knockdown of numerous genes encoding the components of general transcription pathway or its regulatory factors leads to a significant reduction in the E2 cell cycle length but an increase in cell cycle length of the remaining cells, indicating a differential requirement of transcription for division timing between the two. Analysis of lineage-specific RNA-seq data demonstrates an earlier onset of transcription in endoderm than in other germ layers, the timing of which coincides with the birth of E2, supporting the notion that the endoderm-specific delay in E2 division timing demands robust zygotic transcription. The reduction in E2 cell cycle length is frequently associated with cell migration defect and gastrulation failure. The results suggest that a tissue-specific transcriptional activation is required to coordinate fate differentiation, division timing, and cell migration to ensure proper development. PMID:27056332

Inactivation of IkappaBbeta by the tax protein of human T-cell leukemia virus type 1: a potential mechanism for constitutive induction of NF-kappaB.

PubMed

McKinsey, T A; Brockman, J A; Scherer, D C; Al-Murrani, S W; Green, P L; Ballard, D W

1996-05-01

In resting T lymphocytes, the transcription factor NF-kappaB is sequestered in the cytoplasm via interactions with members of the I kappa B family of inhibitors, including IkappaBalpha and IkappaBbeta. During normal T-cell activation, IkappaBalpha is rapidly phosphorylated, ubiquitinated, and degraded by the 26S proteasome, thus permitting the release of functional NF-kappaB. In contrast to its transient pattern of nuclear induction during an immune response, NF-kappaB is constitutively activated in cells expressing the Tax transforming protein of human T-cell leukemia virus type I (HTLV-1). Recent studies indicate that HTLV-1 Tax targets IkappaBalpha to the ubiquitin-proteasome pathway. However, it remains unclear how this viral protein induces a persistent rather than transient NF-kappaB response. In this report, we provide evidence that in addition to acting on IkappaBalpha, Tax stimulates the turnover Of IkappaBbeta via a related targeting mechanism. Like IkappaBalpha, Tax-mediated breakdown of IkappaBbeta in transfected T lymphocytes is blocked either by cell-permeable proteasome inhibitors or by mutation Of IkappaBbeta at two serine residues present within its N-terminal region. Despite the dual specificity of HTLV-1 Tax for IkappaBalpha and IkappaBbeta at the protein level, Tax selectively stimulates NF-kappaB-directed transcription of the IkappaBalpha gene. Consequently, IkappaBbeta protein expression is chronically downregulated in HTLV-1-infected T lymphocytes. These findings with IkappaBbeta provide a potential mechanism for the constitutive activation of NF-kappaB in Tax-expressing cells.

27 CFR 19.21 - Tax.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 27 Alcohol, Tobacco Products and Firearms 1 2010-04-01 2010-04-01 false Tax. 19.21 Section 19.21 Alcohol, Tobacco Products and Firearms ALCOHOL AND TOBACCO TAX AND TRADE BUREAU, DEPARTMENT OF THE TREASURY LIQUORS DISTILLED SPIRITS PLANTS Taxes Gallonage Taxes § 19.21 Tax. (a) A tax is imposed by 26 U.S...

Stimulation of the human immunodeficiency virus type 1 enhancer by the human T-cell leukemia virus type I tax gene product involves the action of inducible cellular proteins.

PubMed

Böhnlein, E; Siekevitz, M; Ballard, D W; Lowenthal, J W; Rimsky, L; Bogérd, H; Hoffman, J; Wano, Y; Franza, B R; Greene, W C

1989-04-01

The human immunodeficiency virus type 1 (HIV-1) preferentially infects CD4+ T lymphocytes and may exist as a latent provirus within these cells for extended periods. The transition to a productive retroviral infection results in T-cell death and clinically may lead to the acquired immune deficiency syndrome. Accelerated production of infectious HIV-1 virions appears to be closely linked to a heightened state of T-cell activation. The transactivator (Tax) protein of the type I human T-cell leukemia virus (HTLV-I) can produce such an activated T-cell phenotype and augments activity of the HIV-1 long terminal repeat. One Tax-responsive region within the HIV-1 long terminal repeat has been mapped to a locus composed of two 10-base-pair direct repeats sharing homology with the binding site for the eucaryotic transcription factor NF-kappaB (GGGACTTTCC). Tax-expressing Jurkat T cells contain one or more inducible cellular proteins that specifically associate with the HIV-1 enhancer at these binding sites. Microscale DNA affinity precipitation assays identified a Tax-inducible 86-kilodalton protein, HIVEN86A, as one of these HIV-1 enhancer-binding factors. The interaction of HIVEN86A, and presumably other cellular proteins, with the HIV-1 enhancer appears functionally important as oligonucleotides corresponding to this enhancer were sufficient to impart Tax inducibility to an unresponsive heterologous promoter. These findings suggest that the Tax-inducible cellular protein HIVEN86A plays an important role in the transcriptional activation of the HIV-1 enhancer. These specific protein-DNA interactions may also be important for the transition of HIV-1 from a latent to a productive mode of infection. Furthermore, these findings highlight an intriguing biological interplay between HTLV-1 and HIV-1 through a cellular transcriptional pathway that is normally involved in T-cell activation and growth.

Tax Tips for Forest Landowners for the 2006 Tax Year

Treesearch

Linda Wang; John L. Greene

2006-01-01

This bulletin summarizes key federal income tax provisions related to owning and managing forest land. It is current as of December 1, 2006, and supercedes Management Bulletin R8-MB 126. But it is only an introduction. Consult the references for more complete information on the topics, and consult your tax and legal advisers for advice on your particular tax situation...

The Helicase Aquarius/EMB-4 Is Required to Overcome Intronic Barriers to Allow Nuclear RNAi Pathways to Heritably Silence Transcription.

PubMed

Akay, Alper; Di Domenico, Tomas; Suen, Kin M; Nabih, Amena; Parada, Guillermo E; Larance, Mark; Medhi, Ragini; Berkyurek, Ahmet C; Zhang, Xinlian; Wedeles, Christopher J; Rudolph, Konrad L M; Engelhardt, Jan; Hemberg, Martin; Ma, Ping; Lamond, Angus I; Claycomb, Julie M; Miska, Eric A

2017-08-07

Small RNAs play a crucial role in genome defense against transposable elements and guide Argonaute proteins to nascent RNA transcripts to induce co-transcriptional gene silencing. However, the molecular basis of this process remains unknown. Here, we identify the conserved RNA helicase Aquarius/EMB-4 as a direct and essential link between small RNA pathways and the transcriptional machinery in Caenorhabditis elegans. Aquarius physically interacts with the germline Argonaute HRDE-1. Aquarius is required to initiate small-RNA-induced heritable gene silencing. HRDE-1 and Aquarius silence overlapping sets of genes and transposable elements. Surprisingly, removal of introns from a target gene abolishes the requirement for Aquarius, but not HRDE-1, for small RNA-dependent gene silencing. We conclude that Aquarius allows small RNA pathways to compete for access to nascent transcripts undergoing co-transcriptional splicing in order to detect and silence transposable elements. Thus, Aquarius and HRDE-1 act as gatekeepers coordinating gene expression and genome defense. Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

State Tax Capacity and the Representative Tax System.

ERIC Educational Resources Information Center

Lucke, Robert B.

1984-01-01

Discusses the merit of using the Representative Tax System to measure state fiscal capacity instead of the traditional measure of per capita income. The conclusion is that the Representative Tax System can play a major role in determining the allocation of federal grants. (MJL)

HTLV-I Tax-dependent and -independent events associated with immortalization of human primary T lymphocytes

PubMed Central

Bellon, Marcia; Baydoun, Hicham H.; Yao, Yuan

2010-01-01

Human T-cell leukemia virus type I (HTLV-I)–associated malignancies are seen in a small percentage of infected persons. Although in vitro immortalization by HTLV-I virus is very efficient, we report that Tax has poor oncogenic activity in human primary T cells and that immortalization by Tax is rare. Sustained telomerase activity represents one of the oncogenic steps required for Tax-mediated immortalization. Tax expression was required for the growth of primary T cells, but was not sufficient to propel T cells into cell cycle in the absence of exogenous interleukin-2 (IL-2). Tax was sufficient to activate the phosphoinositide-3 kinase (PI3K)/Akt pathway as shown by down regulation of Src homology phosphatase-1 and increased phosphorylation of Akt. We also found disruption of putative tumor suppressors IL-16 and translocated promoter region (TPR) in Tax-immortalized and HTLV-I–transformed cell lines. Our results confirmed previous observations that Tax activates the anaphase-promoting complex. However, Tax did not affect the mitotic spindle checkpoint, which was also functional in HTLV-I–transformed cells. These data provide a better understanding of Tax functions in human T cells, and highlight the limitations of Tax, suggesting that other viral proteins are key to T-cell transformation and development of adult T-cell leukemia. PMID:20093405

Transcriptional profiling suggests that multiple metabolic adaptations are required for effective proliferation of Pseudomonas aeruginosa in jet fuel.

PubMed

Gunasekera, Thusitha S; Striebich, Richard C; Mueller, Susan S; Strobel, Ellen M; Ruiz, Oscar N

2013-01-01

Fuel is a harsh environment for microbial growth. However, some bacteria can grow well due to their adaptive mechanisms. Our goal was to characterize the adaptations required for Pseudomonas aeruginosa proliferation in fuel. We have used DNA-microarrays and RT-PCR to characterize the transcriptional response of P. aeruginosa to fuel. Transcriptomics revealed that genes essential for medium- and long-chain n-alkane degradation including alkB1 and alkB2 were transcriptionally induced. Gas chromatography confirmed that P. aeruginosa possesses pathways to degrade different length n-alkanes, favoring the use of n-C11-18. Furthermore, a gamut of synergistic metabolic pathways, including porins, efflux pumps, biofilm formation, and iron transport, were transcriptionally regulated. Bioassays confirmed that efflux pumps and biofilm formation were required for growth in jet fuel. Furthermore, cell homeostasis appeared to be carefully maintained by the regulation of porins and efflux pumps. The Mex RND efflux pumps were required for fuel tolerance; blockage of these pumps precluded growth in fuel. This study provides a global understanding of the multiple metabolic adaptations required by bacteria for survival and proliferation in fuel-containing environments. This information can be applied to improve the fuel bioremediation properties of bacteria.

Human T-lymphotropic virus type 1-infected cells secrete exosomes that contain Tax protein.

PubMed

Jaworski, Elizabeth; Narayanan, Aarthi; Van Duyne, Rachel; Shabbeer-Meyering, Shabana; Iordanskiy, Sergey; Saifuddin, Mohammed; Das, Ravi; Afonso, Philippe V; Sampey, Gavin C; Chung, Myung; Popratiloff, Anastas; Shrestha, Bindesh; Sehgal, Mohit; Jain, Pooja; Vertes, Akos; Mahieux, Renaud; Kashanchi, Fatah

2014-08-08

Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis. The HTLV-1 transactivator protein Tax controls many critical cellular pathways, including host cell DNA damage response mechanisms, cell cycle progression, and apoptosis. Extracellular vesicles called exosomes play critical roles during pathogenic viral infections as delivery vehicles for host and viral components, including proteins, mRNA, and microRNA. We hypothesized that exosomes derived from HTLV-1-infected cells contain unique host and viral proteins that may contribute to HTLV-1-induced pathogenesis. We found exosomes derived from infected cells to contain Tax protein and proinflammatory mediators as well as viral mRNA transcripts, including Tax, HBZ, and Env. Furthermore, we observed that exosomes released from HTLV-1-infected Tax-expressing cells contributed to enhanced survival of exosome-recipient cells when treated with Fas antibody. This survival was cFLIP-dependent, with Tax showing induction of NF-κB in exosome-recipient cells. Finally, IL-2-dependent CTLL-2 cells that received Tax-containing exosomes were protected from apoptosis through activation of AKT. Similar experiments with primary cultures showed protection and survival of peripheral blood mononuclear cells even in the absence of phytohemagglutinin/IL-2. Surviving cells contained more phosphorylated Rb, consistent with the role of Tax in regulation of the cell cycle. Collectively, these results suggest that exosomes may play an important role in extracellular delivery of functional HTLV-1 proteins and mRNA to recipient cells. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.

Tax-Based Educational Equity: A New Approach to School Finance Reform.

ERIC Educational Resources Information Center

Cooper, Bruce S.; And Others

A new argument is made for school finance equalization, based not on "equal protection" or "equal educational opportunity," but on constitutional requirements for tax equity in New Hampshire. Since inequalities in school finance are a taxation problem, they call for tax reform. The analyses rest on four points: (1) that…

Intermediate tax sanctions: an overview.

PubMed

Peregrine, M W

1997-07-01

New federal tax law applies intermediate tax sanctions when tax-exempt organizations enter into so-called excess benefit transactions with corporate insiders. The sanctions take the form of a two-tiered penalty excise tax, which is assessed not on the tax-exempt organization itself but on the insider who receives the excess benefit and the organizational managers and board members who knowingly participate in an improper transaction. The intermediate tax sanctions, therefore, present tax-planning challenges for tax-exempt hospitals and integrated delivery systems as well as for 501(c)(4) HMOs. Forthcoming treasury regulations are expected to add clarity to the new law.

Simian virus 40 major late promoter: an upstream DNA sequence required for efficient in vitro transcription.

PubMed Central

Brady, J; Radonovich, M; Thoren, M; Das, G; Salzman, N P

1984-01-01

We have previously identified an 11-base DNA sequence, 5'-G-G-T-A-C-C-T-A-A-C-C-3' (simian virus 40 [SV40] map position 294 to 304), which is important in the control of SV40 late RNA expression in vitro and in vivo (Brady et al., Cell 31:625-633, 1982). We report here the identification of another domain of the SV40 late promoter. A series of mutants with deletions extending from SV40 map position 0 to 300 was prepared by nuclease BAL 31 treatment. The cloned templates were then analyzed for efficiency and accuracy of late SV40 RNA expression in the Manley in vitro transcription system. Our studies showed that, in addition to the promoter domain near map position 300, there are essential DNA sequences between nucleotide positions 74 and 95 that are required for efficient expression of late SV40 RNA. Included in this SV40 DNA sequence were two of the six GGGCGG SV40 repeat sequences and an 11-nucleotide segment which showed strong homology with the upstream sequences required for the efficient in vitro and in vivo expression of the histone H2A gene. This upstream promoter sequence supported transcription with the same efficiency even when it was moved 72 nucleotides closer to the major late cap site. In vitro promoter competition analysis demonstrated that the upstream promoter sequence, independent of the 294 to 304 promoter element, is capable of binding polymerase-transcription factors required for SV40 late gene transcription. Finally, we show that DNA sequences which control the specificity of RNA initiation at nucleotide 325 lie downstream of map position 294. Images PMID:6321950

Provision of community benefits by tax-exempt U.S. hospitals.

PubMed

Young, Gary J; Chou, Chia-Hung; Alexander, Jeffrey; Lee, Shoou-Yih Daniel; Raver, Eli

2013-04-18

The Patient Protection and Affordable Care Act (ACA) requires tax-exempt hospitals to conduct assessments of community needs and address identified needs. Most tax-exempt hospitals will need to meet this requirement by the end of 2013. We conducted a national study of the level and pattern of community benefits that tax-exempt hospitals provide. The study comprised more than 1800 tax-exempt hospitals, approximately two thirds of all such institutions. We used reports that hospitals filed with the Internal Revenue Service for fiscal year 2009 that provide expenditures for seven types of community benefits. We combined these reports with other data to examine whether institutional, community, and market characteristics are associated with the provision of community benefits by hospitals. Tax-exempt hospitals spent 7.5% of their operating expenses on community benefits during fiscal year 2009. More than 85% of these expenditures were devoted to charity care and other patient care services. Of the remaining community-benefit expenditures, approximately 5% were devoted to community health improvements that hospitals undertook directly. The rest went to education in health professions, research, and contributions to community groups. The level of benefits provided varied widely among the hospitals (hospitals in the top decile devoted approximately 20% of operating expenses to community benefits; hospitals in the bottom decile devoted approximately 1%). This variation was not accounted for by indicators of community need. In 2009, tax-exempt hospitals varied markedly in the level of community benefits provided, with most of their benefit-related expenditures allocated to patient care services. Little was spent on community health improvement.

26 CFR 301.6014-1 - Income tax return-tax not computed by taxpayer.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 18 2010-04-01 2010-04-01 false Income tax return-tax not computed by taxpayer. 301.6014-1 Section 301.6014-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY... Records § 301.6014-1 Income tax return—tax not computed by taxpayer. For provisions relating to the...

Regulation of HTLV-1 Tax Stability, Cellular Trafficking and NF-κB Activation by the Ubiquitin-Proteasome Pathway

PubMed Central

Lavorgna, Alfonso; Harhaj, Edward William

2014-01-01

Human T-cell leukemia virus type 1 (HTLV-1) is a complex retrovirus that infects CD4+ T cells and causes adult T-cell leukemia/lymphoma (ATLL) in 3%–5% of infected individuals after a long latent period. HTLV-1 Tax is a trans-activating protein that regulates viral gene expression and also modulates cellular signaling pathways to enhance T-cell proliferation and cell survival. The Tax oncoprotein promotes T-cell transformation, in part via constitutive activation of the NF-κB transcription factor; however, the underlying mechanisms remain unknown. Ubiquitination is a type of post-translational modification that occurs in a three-step enzymatic cascade mediated by E1, E2 and E3 enzymes and regulates protein stability as well as signal transduction, protein trafficking and the DNA damage response. Emerging studies indicate that Tax hijacks the ubiquitin machinery to activate ubiquitin-dependent kinases and downstream NF-κB signaling. Tax interacts with the E2 conjugating enzyme Ubc13 and is conjugated on C-terminal lysine residues with lysine 63-linked polyubiquitin chains. Tax K63-linked polyubiquitination may serve as a platform for signaling complexes since this modification is critical for interactions with NEMO and IKK. In addition to NF-κB signaling, mono- and polyubiquitination of Tax also regulate its subcellular trafficking and stability. Here, we review recent advances in the diverse roles of ubiquitin in Tax function and how Tax usurps the ubiquitin-proteasome pathway to promote oncogenesis. PMID:25341660

Assessing Patterns of Alcohol Taxes Produced by Various Types of Excise Tax Methods--A Simulation Study.

PubMed

Sornpaisarn, Bundit; Kaewmungkun, Chuthaporn; Rehm, Jürgen

2015-11-01

To examine patterns of tax burdens produced by specific, ad valorem, and various types of combination taxations. One hundred unique hypothetical alcoholic beverages were mathematically simulated based on the amount of ethanol and perceived-qualities contained. Second, beverages were assigned values of various costs and tax rates, and third, patterns of tax burden were assessed per unit of ethanol produced by each type of tax method. Different tax methods produced different tax burdens per unit of ethanol for different alcoholic beverages. The tax burden produced by the ad valorem tax resulted in a lower tax burden for low perceived-quality alcoholic beverages. The specific tax method showed the same tax burden for both low and high perceived-quality alcoholic beverages. However, high perceived-quality beverages benefited from a lower tax burden per beverage price. Lastly, the combination tax method resulted in a lower tax burden for medium perceived-quality alcoholic beverages. Under the oligopoly market, ad valorem taxation encourages consumption of low perceived-quality beverages; specific taxation encourages consumption of high perceived-quality beverages; and combination tax methods encourage consumption of medium perceived-quality beverages. © The Author 2015. Medical Council on Alcohol and Oxford University Press. All rights reserved.

Implications of the Supplemental Nutrition Assistance Program Tax Exemption on Sugar-Sweetened Beverage Taxes

PubMed Central

2015-01-01

US state and local governments are debating sugar-sweetened beverage excise taxes to support public health. A related issue is whether such taxes would apply to beverage purchases made by Supplemental Nutrition Assistance Program (SNAP) participants. Federal law proscribes states from collecting excise taxes on SNAP purchases, but the law is confined to taxes at the point of sale. I provide legal analysis and recommendations for policymakers to enact taxes that are not subject to the SNAP tax exemption to potentially deter consumption by all consumers. PMID:26378844

Tuition Tax Credits. Issuegram 19.

ERIC Educational Resources Information Center

Augenblick, John; McGuire, Kent

Approaches for using the federal income tax system to aid families of pupils attending private schools include: tax credits, tax deductions, tax deferrals, and education savings incentives. Tax credit structures can be made refundable and made sensitive to taxpayers' income levels, the level of education expenditures, and designated costs.…

A Non-SUMOylated Tax Protein Is Still Functional for NF-κB Pathway Activation

PubMed Central

Pène, Sabrina; Waast, Laetitia; Bonnet, Amandine; Bénit, Laurence

2014-01-01

ABSTRACT Whether NF-κB promoter transactivation by the human T-cell leukemia virus type 1 (HTLV-1) Tax protein requires Tax SUMOylation is still a matter of debate. In this study, we revisited the role of Tax SUMOylation using a strategy based on the targeting of Ubc9, the unique E2 SUMO-conjugating enzyme. We show that either a catalytically inactive form of Ubc9 (Ubc9-C93S) or Ubc9 small interfering RNA (siRNA) dramatically reduces Tax conjugation to endogenous SUMO-1 or SUMO-2/3, demonstrating that as expected, Tax SUMOylation is under the control of the catalytic activity of Ubc9. We further report that a non-SUMOylated Tax protein produced in 293T cells is still able to activate either a transfected or an integrated NF-κB reporter promoter and to induce expression of an NF-κB-regulated endogenous gene. Importantly, blocking Ubc9 activity in T cells also results in the production of a non-SUMOylated Tax that is still fully functional for the activation of a NF-κB promoter. These results provide the definitive evidence that Tax SUMOylation is not required for NF-κB-driven gene induction. IMPORTANCE Human T-cell leukemia virus type 1 is able to transform CD4+ T lymphocytes. The viral oncoprotein Tax plays a key role in this process by promoting cell proliferation and survival, mainly through permanent activation of the NF-κB pathway. Elucidating the molecular mechanisms involved in NF-κB pathway activation by Tax is therefore a key issue to understand HTLV-1-mediated transformation. Tax SUMOylation was initially proposed to be critical for Tax-induced NF-κB promoter activation, which was challenged by our later observation that a low-level-SUMOylated Tax mutant was still functional for activation of NF-κB promoters. To clarify the role of Tax SUMOylation, we set up a new approach based on the inhibition of the SUMOylation machinery in Tax-expressing cells. We show that blocking the SUMO-conjugating enzyme Ubc9 abolishes Tax SUMOylation and that a non

A non-SUMOylated tax protein is still functional for NF-κB pathway activation.

PubMed

Pène, Sabrina; Waast, Laetitia; Bonnet, Amandine; Bénit, Laurence; Pique, Claudine

2014-09-01

Whether NF-κB promoter transactivation by the human T-cell leukemia virus type 1 (HTLV-1) Tax protein requires Tax SUMOylation is still a matter of debate. In this study, we revisited the role of Tax SUMOylation using a strategy based on the targeting of Ubc9, the unique E2 SUMO-conjugating enzyme. We show that either a catalytically inactive form of Ubc9 (Ubc9-C93S) or Ubc9 small interfering RNA (siRNA) dramatically reduces Tax conjugation to endogenous SUMO-1 or SUMO-2/3, demonstrating that as expected, Tax SUMOylation is under the control of the catalytic activity of Ubc9. We further report that a non-SUMOylated Tax protein produced in 293T cells is still able to activate either a transfected or an integrated NF-κB reporter promoter and to induce expression of an NF-κB-regulated endogenous gene. Importantly, blocking Ubc9 activity in T cells also results in the production of a non-SUMOylated Tax that is still fully functional for the activation of a NF-κB promoter. These results provide the definitive evidence that Tax SUMOylation is not required for NF-κB-driven gene induction. Human T-cell leukemia virus type 1 is able to transform CD4(+) T lymphocytes. The viral oncoprotein Tax plays a key role in this process by promoting cell proliferation and survival, mainly through permanent activation of the NF-κB pathway. Elucidating the molecular mechanisms involved in NF-κB pathway activation by Tax is therefore a key issue to understand HTLV-1-mediated transformation. Tax SUMOylation was initially proposed to be critical for Tax-induced NF-κB promoter activation, which was challenged by our later observation that a low-level-SUMOylated Tax mutant was still functional for activation of NF-κB promoters. To clarify the role of Tax SUMOylation, we set up a new approach based on the inhibition of the SUMOylation machinery in Tax-expressing cells. We show that blocking the SUMO-conjugating enzyme Ubc9 abolishes Tax SUMOylation and that a non-SUMOylated Tax still

Taxing Matters: College Aid, Tax Policy & Equal Opportunity.

ERIC Educational Resources Information Center

Education Resources Inst., Boston, MA.

This report uses government data to review current, past, and proposed tax-based policies and programs to promote college affordability as well as need-based grant aid. Tax-incentive-based programs include savings bonds for education, employer-provided educational assistance, state college savings plans, deductibility of student loan interest,…

26 CFR 1.6655-2T - Safe harbor for certain installments of tax due before July 1, 1987 (temporary).

Code of Federal Regulations, 2010 CFR

2010-04-01

..., DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES Additions to the Tax, Additional... estimated tax is being paid may use that carryover to reduce the annualized taxable income referred to in... payment (“the subsequent installment payment”) of estimated tax required to be made after the last payment...

26 CFR 1.6016-1 - Declarations of estimated income tax by corporations.

Code of Federal Regulations, 2011 CFR

2011-04-01

... corporations. 1.6016-1 Section 1.6016-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY... of estimated income tax by corporations. (a) Requirement. For taxable years ending on or after December 31, 1955, a declaration of estimated tax shall be made by every corporation (including...

Tax planning strategies for physicians.

PubMed

Pope, Thomas R; Schwartz, Richard W

2002-07-01

The development of tax reduction strategies is a critical aspect of both corporate and personal financial planning because taxes represent the largest annual expenditure for the majority of Americans. The categories of tax reduction strategies discussed include charitable-giving techniques, ways to maximize business deductions, shifting income to family members, education tax incentives, retirement planning, and small business tax considerations. One use for these tax savings is the enhancement of a corporation's capabilities to provide services to patients.

Tax Rates and Tax Evasion: Evidence from "Missing Imports" in China.

ERIC Educational Resources Information Center

Fisman, Raymond; Wei, Shang-Jin

2004-01-01

Tax evasion, by its very nature, is difficult to observe. We quantify the effects of tax rates on tax evasion by examining the relationship in China between the tariff schedule and the "evasion gap," which we define as the difference between Hong Kong's reported exports to China at the product level and China's reported imports from Hong…

77 FR 37362 - Implementation of the Middle Class Tax Relief and Job Creation Act of 2012; Establishment of a...

Federal Register 2010, 2011, 2012, 2013, 2014

2012-06-21

...] Implementation of the Middle Class Tax Relief and Job Creation Act of 2012; Establishment of a Public Safety... public safety answering points (PSAPs) as required by the ``Middle Class Tax Relief and Job Creation Act... Objectives of, the Proposed Rules 21. The ``Middle Class Tax Relief and Job Creation Act of 2012'' requires...

Myocyte enhancer factor (MEF)-2 plays essential roles in T-cell transformation associated with HTLV-1 infection by stabilizing complex between Tax and CREB.

PubMed

Jain, Pooja; Lavorgna, Alfonso; Sehgal, Mohit; Gao, Linlin; Ginwala, Rashida; Sagar, Divya; Harhaj, Edward W; Khan, Zafar K

2015-02-27

The exact molecular mechanisms regarding HTLV-1 Tax-mediated viral gene expression and CD4 T-cell transformation have yet to be fully delineated. Herein, utilizing virus-infected primary CD4+ T cells and the virus-producing cell line, MT-2, we describe the involvement and regulation of Myocyte enhancer factor-2 (specifically MEF-2A) during the course of HTLV-1 infection and associated disease syndrome. Inhibition of MEF-2 expression by shRNA and its activity by HDAC9 led to reduced viral replication and T-cell transformation in correlation with a heightened expression of MEF-2 in ATL patients. Mechanistically, MEF-2 was recruited to the viral promoter (LTR, long terminal repeat) in the context of chromatin, and constituted Tax/CREB transcriptional complex via direct binding to the HTLV-1 LTR. Furthermore, an increase in MEF-2 expression was observed upon infection in an extent similar to CREB (known Tax-interacting transcription factor), and HATs (p300, CBP, and p/CAF). Confocal imaging confirmed MEF-2 co-localization with Tax and these proteins were also shown to interact by co-immunoprecipitation. MEF-2 stabilization of Tax/CREB complex was confirmed by a novel promoter-binding assay that highlighted the involvement of NFAT (nuclear factor of activated T cells) in this process via Tax-mediated activation of calcineurin (a calcium-dependent serine-threonine phosphatase). MEF-2-integrated signaling pathways (PI3K/Akt, NF-κB, MAPK, JAK/STAT, and TGF-β) were also activated during HTLV-1 infection of primary CD4+ T cells, possibly regulating MEF-2 activity. We demonstrate the involvement of MEF-2 in Tax-mediated LTR activation, viral replication, and T-cell transformation in correlation with its heightened expression in ATL patients through direct binding to DNA within the HTLV-1 LTR.

Property-tax incentives for implementing soil-conservation programs under constitutional taxing limitations

DOE Office of Scientific and Technical Information (OSTI.GOV)

Massey, D.T.; Silver, M.B.

1982-01-01

This article describes how property-tax incentives can be used to implement soil-conservation programs on agricultural and open-space lands under the differential-assessment statutes and other exceptions to constitutional limitations on taxation powers. The article describes restrictions imposed on taxing powers by the constitutional uniformity clauses and methods for circumventing those limitations; various property-tax incentives available for conservation programs; types of differential or use-value assessments providing property-tax relief for farm, forest, and open-space land preservation; eligibility of lands for differential assessments; methods available to landowners for participation in differential assessments; and determination of value under differential assessment. The article next details howmore » each of the three primary types of differential or use-value assessment statutes for farm, forest, and open-space land preservation provides exceptions to the uniformity clauses for property tax incentives to implement soil-conservation programs. Other methods available for providing exceptions to the uniformity clauses to permit property-tax incentives are also described for each of the three states. Each of these states has statutes giving favorable tax treatment to certain types of property, such as pollution-abatement equipment, alternative energy-producing devices, and even country clubs. These statutes can be used as examples of finding a constitutional method for providing favorabe tax treatment to promote participation in soil-conservation programs.« less

77 FR 43077 - Federal Acquisition Regulation; Information Collection; North Carolina Sales Tax Certification

Federal Register 2010, 2011, 2012, 2013, 2014

2012-07-23

...; Information Collection; North Carolina Sales Tax Certification AGENCY: Department of Defense (DOD), General... information collection requirement concerning North Carolina sales tax certification. Public comments are particularly invited on: Whether this collection of information is necessary for the proper performance of...

18 CFR 367.102 - Accounts 408.1 and 408.2, Taxes other than income taxes.

Code of Federal Regulations, 2010 CFR

2010-04-01

... COMPANY ACT OF 2005, FEDERAL POWER ACT AND NATURAL GAS ACT UNIFORM SYSTEM OF ACCOUNTS FOR CENTRALIZED... taxes, state unemployment insurance, franchise taxes, Federal excise taxes, social security taxes, and...

26 CFR 521.115 - Credit against United States tax liability for Danish tax.

Code of Federal Regulations, 2010 CFR

2010-04-01

... (CONTINUED) REGULATIONS UNDER TAX CONVENTIONS DENMARK General Income Tax Taxation of Nonresident Aliens Who... liability for Danish tax. For the purpose of avoidance of double taxation, Article XV provides that, on the...

26 CFR 521.115 - Credit against United States tax liability for Danish tax.

Code of Federal Regulations, 2011 CFR

2011-04-01

... (CONTINUED) REGULATIONS UNDER TAX CONVENTIONS DENMARK General Income Tax Taxation of Nonresident Aliens Who... liability for Danish tax. For the purpose of avoidance of double taxation, Article XV provides that, on the...

Employment impacts of alcohol taxes.

PubMed

Wada, Roy; Chaloupka, Frank J; Powell, Lisa M; Jernigan, David H

2017-12-01

There is strong scientific evidence supporting the effectiveness of increasing alcohol taxes for reducing excessive alcohol consumption and related problems. Opponents have argued that alcohol tax increases lead to job losses. However, there has been no comprehensive economic analysis of the impact of alcohol taxes on employment. To fill this gap, a regional macroeconomic simulation model was used to assess the net impact of two hypothetical alcohol tax increases (a 5-cent per drink excise tax increase and a 5% sales tax increase on beer, wine, and distilled spirits, respectively) on employment in Arkansas, Florida, Massachusetts, New Mexico, and Wisconsin. The model accounted for changes in alcohol demand, average state income, and substitution effects. The employment impact of spending the new tax revenue on general expenditures versus health care was also assessed. Simulation results showed that a 5-cent per drink additional excise tax on alcoholic beverages with new tax revenues allocated to general expenditures increased net employment in Arkansas (802 jobs); Florida (4583 jobs); Massachusetts (978 jobs); New Mexico (653 jobs); and Wisconsin (1167 jobs). A 5% additional sales tax also increased employment in Arkansas (789 jobs; Florida (4493 jobs); Massachusetts (898 jobs); New Mexico (621 jobs); and Wisconsin (991 jobs). Using new alcohol tax revenues to fund health care services resulted in slightly lower net increases in state employment. The overall economic impact of alcohol tax increases cannot be fully assessed without accounting for the job gains resulting from additional tax revenues. Copyright © 2017 Elsevier Inc. All rights reserved.

Harmonized sales tax a taxing issue for MDs in Atlantic Canada

PubMed Central

Robb, N

1997-01-01

Physicians in 3 atlantic provinces say the linking of provincial sales taxes with the GST exacerbates the inequity physicians face because it yet again adds to their overhead costs. Physicians in Nova Scotia have already won an annual rebate to compensate them for the heavier tax burden. Doctors in the Maritimes warn that heavier taxes make recruiting there even more difficult. PMID:9371073

41 CFR 105-55.024 - Consideration of tax consequences to the Government.

Code of Federal Regulations, 2010 CFR

2010-07-01

... consequences to the Government. 105-55.024 Section 105-55.024 Public Contracts and Property Management Federal... consequences to the Government. In negotiating a compromise, the General Services Administration (GSA) may consider the tax consequences to the Government. In particular, GSA may consider requiring a waiver of tax...

77 FR 13385 - Identification of Interstate Motor Vehicles: New York City, Cook County, and New Jersey Tax...

Federal Register 2010, 2011, 2012, 2013, 2014

2012-03-06

...-0271] Identification of Interstate Motor Vehicles: New York City, Cook County, and New Jersey Tax Identification Requirements; Petition for Reconsideration. AGENCY: Federal Motor Carrier Safety Administration... Commercial Motor Vehicle Tax (CMV Tax) is preempted. Federal law prohibits States and their political...

26 CFR 48.6416(a)-3 - Credit or refund of manufacturers tax under chapter 32.

Code of Federal Regulations, 2010 CFR

2010-04-01

... total inventory, by model number and quantity, of all such articles purchased tax-paid and held for sale... article is not subject to tax under chapter 32. (C) Inventory requirement. The inventory shall not include... the price of the article with respect to which it was imposed nor collected the amount of the tax from...

48 CFR 2131.205-41 - Taxes.

Code of Federal Regulations, 2010 CFR

2010-10-01

... GROUP LIFE INSURANCE FEDERAL ACQUISITION REGULATION GENERAL CONTRACTING REQUIREMENTS CONTRACT COST PRINCIPLES AND PROCEDURES Contracts With Commercial Organizations 2131.205-41 Taxes. (a) FAR 31.205-41, as modified in paragraphs (b) through (e), is applicable to contracts in the FEGLI Program. (b) As long as 5 U...

Purification of Xenopus laevis mitochondrial RNA polymerase and identification of a dissociable factor required for specific transcription

DOE Office of Scientific and Technical Information (OSTI.GOV)

Bogenhagen, D.F.; Insdorf, N.F.

1988-07-01

The Xenopus laevis mitochondrial RNA (mtRNA) polymerase was purified to near homogeneity with an overall yield approaching 50%. The major polypeptides in the final fraction were a doublet of proteins of approximately 140 kilodaltons that copurified with the mtRNA polymerase activity. It appeared likely that the smaller polypeptide is a breakdown product of the larger one. The highly purified polymerase was active in nonspecific transcription but required a dissociable factor for specific transcription of X. laevis mtDNA. The factor could be resolved from mtRNA polymerase by hydrophobic chromatography and had a sedimentation coefficient of 3.0 S. The transcription factor elutedmore » from both the hydrophobic column and a Mono Q anion-exchange column as a single symmetrical peak. The mtRNA polymerase and this factor together are necessary and sufficient for active transcription from four promoters located in a noncoding region of the mtDNA genome between the gene for tRNA/sup Phe/ and the displacement loop.« less

The lymphotoxin promoter is stimulated by HTLV-I tax activation of NF-kappa B in human T-cell lines.

PubMed

Paul, N L; Millet, I; Ruddle, N H

1993-07-01

The HTLV-I transcriptional activator tax was used to gain insight into the mechanism of lymphotoxin (LT; TNF-beta) gene induction. Tax-expressing cell lines produce LT biologic activity. An LT promoter (LT-293) CAT construct that contained an NF-kappa B site was active in the LT-producing C81-66-45 cell line, which contains defective HTLV-I but expresses tax. The observation that a mutated LT-kappa B construct (M1-CAT) was inactive in C81-66-45, confirmed the importance of NF-kappa B in LT gene expression. Tax was transfected into HTLV-I-negative human T-cell lines. Jurkat T cells stably expressing tax contained elevated levels of NF-kappa B that directly bound to the LT-kappa B site. Tax co-transfected with reporter constructs into Jurkat cells maximally activated HTLV-I-LTR-CAT and kappa B-fos-CAT and also activated LT-293 to a lesser extent. In JM T cells, tax induced LT-293 activity by two- to four-fold, though there was no induction of M1-CAT. The increase in LT-293 CAT activity mirrored the increase in LT biologic activity seen under these conditions. These studies, the first to demonstrate induction of LT promoter activity over basal levels, indicate that HTLV-I tax causes low-level activation of both endogenous LT and the LT promoter, at least in part through activation of NF-kappa B.

Tax Tips for Forest Landowners for the 2013 Tax Year

Treesearch

Linda Wang; John Greene

2013-01-01

This annual bulletin provides federal income tax reporting tips to assist forest landowners and their advisers in filing their 2013 income tax returns. The information presented here is current as of Sept. 15, 2013.

76 FR 53818 - Determining the Amount of Taxes Paid for Purposes of the Foreign Tax Credit

Federal Register 2010, 2011, 2012, 2013, 2014

2011-08-30

... Determining the Amount of Taxes Paid for Purposes of the Foreign Tax Credit AGENCY: Internal Revenue Service... of taxes paid for purposes of the foreign tax credit. These regulations address certain highly structured arrangements that produce inappropriate foreign tax credit results. The regulations affect...

Tax-exempt bank loans still an option for providers.

PubMed

Ostlund, Grant; Cheney, John E

2011-07-01

In evaluating the potential for tax-exempt bank financing, healthcare organizations should carefully consider: Pricing. Loan structure. Security requirements (such as financial covenants and default remedies).

26 CFR 301.6011(g)-1 - Disclosure by taxable party to the tax-exempt entity.

Code of Federal Regulations, 2012 CFR

2012-04-01

... entity. 301.6011(g)-1 Section 301.6011(g)-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE... Returns and Records § 301.6011(g)-1 Disclosure by taxable party to the tax-exempt entity. (a) Requirement... prohibited tax shelter transaction. For purposes of section 6011(g), a tax-exempt entity is a party to a...

26 CFR 301.6011(g)-1 - Disclosure by taxable party to the tax-exempt entity.

Code of Federal Regulations, 2014 CFR

2014-04-01

... entity. 301.6011(g)-1 Section 301.6011(g)-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE... Returns and Records § 301.6011(g)-1 Disclosure by taxable party to the tax-exempt entity. (a) Requirement... prohibited tax shelter transaction. For purposes of section 6011(g), a tax-exempt entity is a party to a...

26 CFR 301.6011(g)-1 - Disclosure by taxable party to the tax-exempt entity.

Code of Federal Regulations, 2011 CFR

2011-04-01

... entity. 301.6011(g)-1 Section 301.6011(g)-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE... Returns and Records § 301.6011(g)-1 Disclosure by taxable party to the tax-exempt entity. (a) Requirement... prohibited tax shelter transaction. For purposes of section 6011(g), a tax-exempt entity is a party to a...

26 CFR 301.6011(g)-1 - Disclosure by taxable party to the tax-exempt entity.

Code of Federal Regulations, 2013 CFR

2013-04-01

... entity. 301.6011(g)-1 Section 301.6011(g)-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE... Returns and Records § 301.6011(g)-1 Disclosure by taxable party to the tax-exempt entity. (a) Requirement... prohibited tax shelter transaction. For purposes of section 6011(g), a tax-exempt entity is a party to a...

Myocardin-related transcription factors and SRF are required for cytoskeletal dynamics and experimental metastasis.

PubMed

Medjkane, Souhila; Perez-Sanchez, Cristina; Gaggioli, Cedric; Sahai, Erik; Treisman, Richard

2009-03-01

Rho GTPases control cytoskeletal dynamics through cytoplasmic effectors and regulate transcriptional activation through myocardin-related transcription factors (MRTFs), which are co-activators for serum response factor (SRF). We used RNA interference to investigate the contribution of the MRTF-SRF pathway to cytoskeletal dynamics in MDA-MB-231 breast carcinoma and B16F2 melanoma cells, in which basal MRTF-SRF activity is Rho-dependent. Depletion of MRTFs or SRF reduced cell adhesion, spreading, invasion and motility in culture, without affecting proliferation or inducing apoptosis. MRTF-depleted tumour cell xenografts showed reduced cell motility but proliferated normally. Tumour cells depleted of MRTF or SRF failed to colonize the lung from the bloodstream, being unable to persist after their arrival in the lung. Only a few genes show MRTF-dependent expression in both cell lines. Two of these, MYH9 (NMHCIIa) and MYL9 (MLC2), are also required for invasion and lung colonization. Conversely, expression of activated MAL/MRTF-A increases lung colonization by poorly metastatic B16F0 cells. Actin-based cell behaviour and experimental metastasis thus require Rho-dependent nuclear signalling through the MRTF-SRF network.

76 FR 40946 - WNC Tax Credits 40, LLC, WNC Tax Credits 41, LLC, WNC Housing Tax Credits Manager 2, LLC, WNC...

Federal Register 2010, 2011, 2012, 2013, 2014

2011-07-12

... Credits 40, LLC, WNC Tax Credits 41, LLC, WNC Housing Tax Credits Manager 2, LLC, WNC National Partners... (``Fund 41'') (each a ``Fund,'' and collectively, the ``Funds''), WNC Housing Tax Credits Manager 2, LLC (the ``Manager''), WNC National Partners, LLC (``WNC National Partners'') and WNC & Associates, Inc...

Use of tobacco tax stamps to prevent and reduce illicit tobacco trade--United States, 2014.

PubMed

Chriqui, Jamie; DeLong, Hillary; Gourdet, Camille; Chaloupka, Frank; Edwards, Sarah Matthes; Xu, Xin; Promoff, Gabbi

2015-05-29

Tobacco use is the leading cause of preventable disease and death in the United States. Increasing the unit price on tobacco products is the most effective tobacco prevention and control measure. Illicit tobacco trade (illicit trade) undermines high tobacco prices by providing tobacco users with cheaper-priced alternatives. In the United States, illicit trade primarily occurs when cigarettes are bought from states, jurisdictions, and federal reservation land with lower or no excise taxes, and sold in jurisdictions with higher taxes. Applying tax stamps to tobacco products, which provides documentation that taxes have been paid, is an important tool to combat illicit trade. Comprehensive tax stamping policy, which includes using digital, encrypted ("high-tech") stamps, applying stamps to all tobacco products, and working with tribes on stamping agreements, can further prevent and reduce illicit trade. This report describes state laws governing tax stamps on cigarettes, little cigars (cigarette-sized cigars), roll-your-own tobacco (RYOT), and tribal tobacco sales across the United States as of January 1, 2014, and assesses the extent of comprehensive tobacco tax stamping in the United States. Forty-four states (including the District of Columbia [DC]) applied traditional paper ("low-tech") tax stamps to cigarettes, whereas four authorized more effective high-tech stamps. Six states explicitly required stamps on other tobacco products (i.e., tobacco products other than cigarettes), and in approximately one third of states with tribal lands, tribes required tax stamping to address illicit purchases by nonmembers. No U.S. state had a comprehensive approach to tobacco tax stamping. Enhancing tobacco tax stamping across the country might further prevent and reduce illicit trade in the United States.

26 CFR 1.905-5T - Foreign tax redeterminations and currency translation rules for foreign tax redeterminations...

Code of Federal Regulations, 2010 CFR

2010-04-01

... translation rules for foreign tax redeterminations occurring in taxable years beginning prior to January 1... States § 1.905-5T Foreign tax redeterminations and currency translation rules for foreign tax... translation rules—(1) Foreign taxes paid by the taxpayer and certain foreign taxes deemed paid. Foreign taxes...

Transcriptional activation of peroxisome proliferator-activated receptor-{gamma} requires activation of both protein kinase A and Akt during adipocyte differentiation

DOE Office of Scientific and Technical Information (OSTI.GOV)

Kim, Sang-pil; Ha, Jung Min; Yun, Sung Ji

2010-08-13

Research highlights: {yields} Elevated cAMP activates both PKA and Epac. {yields} PKA activates CREB transcriptional factor and Epac activates PI3K/Akt pathway via Rap1. {yields} Akt modulates PPAR-{gamma} transcriptional activity in concert with CREB. -- Abstract: Peroxisome proliferator-activated receptor-{gamma} (PPAR-{gamma}) is required for the conversion of pre-adipocytes. However, the mechanism underlying activation of PPAR-{gamma} is unclear. Here we showed that cAMP-induced activation of protein kinase A (PKA) and Akt is essential for the transcriptional activation of PPAR-{gamma}. Hormonal induction of adipogenesis was blocked by a phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002), by a protein kinase A (PKA) inhibitor (H89), and by amore » Rap1 inhibitor (GGTI-298). Transcriptional activity of PPAR-{gamma} was markedly enhanced by 3-isobutyl-1-methylxanthine (IBMX), but not insulin and dexamethasone. In addition, IBMX-induced PPAR-{gamma} transcriptional activity was blocked by PI3K/Akt, PKA, or Rap1 inhibitors. 8-(4-Chlorophenylthio)-2'-O-methyl-cAMP (8-pCPT-2'-O-Me-cAMP) which is a specific agonist for exchanger protein directly activated by cAMP (Epac) significantly induced the activation of Akt. Furthermore, knock-down of Akt1 markedly attenuated PPAR-{gamma} transcriptional activity. These results indicate that both PKA and Akt signaling pathways are required for transcriptional activation of PPAR-{gamma}, suggesting post-translational activation of PPAR-{gamma} might be critical step for adipogenic gene expression.« less

Education and Tax Limitations: Evidence from Massachusetts' Proposition 2 1/2.

ERIC Educational Resources Information Center

Ladd, Helen F.; Wilson, Julie Boatright

This paper uses survey data collected during the 2 weeks following the November 4, 1980, election to answer questions concerning how local public education should be funded in the wake of the passing of Proposition 2 1/2, a measure that requires high tax rate cities and towns to reduce property tax levies by at least 15 percent per year until they…

US Supreme Court set to hear oral arguments in Montana coal tax case

DOE Office of Scientific and Technical Information (OSTI.GOV)

Not Available

1981-04-01

Montana defends it 30% coal severance tax as proper compensation for exporting an exhaustible resource, but 11 utilities and four coal companies are suing on constitutional grounds. The suit charges that the tax does not balance costs and benefits and that it represents an effort to export tax burdens. Montana contends that the tax passed in 1975 recognizes the state's long-term needs by requiring that 50% of the revenue be placed in a permanent trust fund for future social and environmental adjustments and questions whether the courts can put a monetary value on these impacts. The plaintiffs see the trustmore » fund as an admission that the tax is excessive and the state's failure to comply with national energy policy. (DCK)« less

48 CFR 29.401-4 - New Mexico gross receipts and compensating tax.

Code of Federal Regulations, 2010 CFR

2010-10-01

... 48 Federal Acquisition Regulations System 1 2010-10-01 2010-10-01 false New Mexico gross receipts... ACQUISITION REGULATION GENERAL CONTRACTING REQUIREMENTS TAXES Contract Clauses 29.401-4 New Mexico gross... Gross Receipts and Compensating Tax Act of the State of New Mexico, Sec. 7-9-3(k) NM SA 1978, and means...

48 CFR 29.401-4 - New Mexico gross receipts and compensating tax.

Code of Federal Regulations, 2012 CFR

2012-10-01

... 48 Federal Acquisition Regulations System 1 2012-10-01 2012-10-01 false New Mexico gross receipts... ACQUISITION REGULATION GENERAL CONTRACTING REQUIREMENTS TAXES Contract Clauses 29.401-4 New Mexico gross... Gross Receipts and Compensating Tax Act of the State of New Mexico, Sec. 7-9-3(k) NM SA 1978, and means...

48 CFR 29.401-4 - New Mexico gross receipts and compensating tax.

Code of Federal Regulations, 2013 CFR

2013-10-01

... 48 Federal Acquisition Regulations System 1 2013-10-01 2013-10-01 false New Mexico gross receipts... ACQUISITION REGULATION GENERAL CONTRACTING REQUIREMENTS TAXES Contract Clauses 29.401-4 New Mexico gross... Gross Receipts and Compensating Tax Act of the State of New Mexico, Sec. 7-9-3(k) NM SA 1978, and means...

48 CFR 29.401-4 - New Mexico gross receipts and compensating tax.

Code of Federal Regulations, 2014 CFR

2014-10-01

... 48 Federal Acquisition Regulations System 1 2014-10-01 2014-10-01 false New Mexico gross receipts... ACQUISITION REGULATION GENERAL CONTRACTING REQUIREMENTS TAXES Contract Clauses 29.401-4 New Mexico gross... Gross Receipts and Compensating Tax Act of the State of New Mexico, Sec. 7-9-3(k) NM SA 1978, and means...

48 CFR 29.401-4 - New Mexico gross receipts and compensating tax.

Code of Federal Regulations, 2011 CFR

2011-10-01

... 48 Federal Acquisition Regulations System 1 2011-10-01 2011-10-01 false New Mexico gross receipts... ACQUISITION REGULATION GENERAL CONTRACTING REQUIREMENTS TAXES Contract Clauses 29.401-4 New Mexico gross... Gross Receipts and Compensating Tax Act of the State of New Mexico, Sec. 7-9-3(k) NM SA 1978, and means...

Myocardin-related transcription factors are required for cardiac development and function

PubMed Central

Mokalled, Mayssa H.; Carroll, Kelli J.; Cenik, Bercin K.; Chen, Beibei; Liu, Ning; Olson, Eric N.; Bassel-Duby, Rhonda

2016-01-01

Myocardin-Related Transcription Factors A and B (MRTF-A and MRTF-B) are highly homologous proteins that function as powerful coactivators of serum response factor (SRF), a ubiquitously expressed transcription factor essential for cardiac development. The SRF/MRTF complex binds to CArG boxes found in the control regions of genes that regulate cytoskeletal dynamics and muscle contraction, among other processes. While SRF is required for heart development and function, the role of MRTFs in the developing or adult heart has not been explored. Through cardiac-specific deletion of MRTF alleles in mice, we show that either MRTF-A or MRTF-B is dispensable for cardiac development and function, whereas deletion of both MRTF-A and MRTF-B causes a spectrum of structural and functional cardiac abnormalities. Defects observed in MRTF-A/B null mice ranged from reduced cardiac contractility and adult onset heart failure to neonatal lethality accompanied by sarcomere disarray. RNA-seq analysis on neonatal hearts identified the most altered pathways in MRTF double knockout hearts as being involved in cytoskeletal organization. Together, these findings demonstrate redundant but essential roles of the MRTFs in maintenance of cardiac structure and function and as indispensible links in cardiac cytoskeletal gene regulatory networks. PMID:26386146

Tax-dependent stimulation of G1 phase-specific cyclin-dependent kinases and increased expression of signal transduction genes characterize HTLV type 1-transformed T cells.

PubMed

Haller, K; Ruckes, T; Schmitt, I; Saul, D; Derow, E; Grassmann, R

2000-11-01

Human T cell leukemia virus protein induces T cells to permanent IL-2-dependent growth. These cells occasionally convert to factor independence. The viral oncoprotein Tax acts as an essential growth factor of transformed lymphocytes and stimulates the cell cycle in the G(1) phase. In T cells and fibroblasts Tax enhances the activity of the cyclin-dependent kinases (CDK) CDK4 and CDK6. These kinases, which require binding to cyclin D isotypes for their activity, control the G(1) phase. Coimmunoprecipitation from these cells revealed that Tax associates with cyclin D3/CDK6, suggesting a direct activation of this kinase. The CDK stimulation may account in part for the mitogenic Tax effect, which causes IL-2-dependent T cell growth by Tax. To address the conversion to IL-2-independent proliferation and to identify overexpressed genes, which contribute to the transformed growth, the gene expression patterns of HTLV-1-transformed T cells were compared with that of peripheral blood lymphocytes. Potentially overexpressed cDNAs were cloned, sequenced, and used to determine the RNA expression. Genes found to be up-regulated are involved in signal transduction (STAT5a, cyclin G(1), c-fgr, hPGT) and also glycoprotein synthesis (LDLC, ribophorin). Many of these are also activated during T cell activation and implicated in the regulation of growth and apoptosis. The transcription factor STAT5a, which is involved in IL-2 signaling, was strongly up-regulated only in IL-2-independent cells, thus suggesting that it contributes to factor-independent growth. Thus, the differentially expressed genes could cooperate with the Tax-induced cell cycle stimulation in the maintenance of IL-2-dependent and IL-2-independent growth of HTLV-transformed lymphocytes.

Deferred compensation for tax-exempt entities.

PubMed

Rich, C; Jenkins, G E

1993-10-01

Many executives in tax-exempt organizations, including healthcare executives, find their tax-advantaged savings opportunities dramatically reduced today compared to previous years. The benefit of employer-sponsored, "qualified" retirement and savings programs has been severely limited by ever-increasing tax restrictions on such plans when they are offered by tax-exempt organizations. And the opportunity for tax-sheltered personal investments has virtually disappeared. One of the last remaining opportunities for tax-advantaged savings in tax-exempt organizations is an employer-sponsored, non-qualified, deferred compensation plan, an option that appears increasingly attractive in light of the recently enacted increased personal tax rates.

The welfare gain from replacing the health insurance tax exclusion with lump-sum tax credits.

PubMed

Liu, Liqun; Rettenmaier, Andrew J; Saving, Thomas R

2011-06-01

This paper analyzes the welfare gain from replacing the tax exclusion of employer-provided health insurance with a lump-sum tax credit. It differs from earlier studies in that we look at the welfare cost of health insurance tax exclusion as coming directly from excessive health insurance rather than from overconsumption of medical care and that we account for the labor market effect of the tax exclusion on welfare. Both differences work to produce a smaller tax reform welfare gain. For a set of mid-range parameter values, the welfare gain is about 21% of current health insurance tax expenditures. In addition, government tax expenditures would fall by 38%, and health insurance spending would fall by 77% after the reform.

75 FR 17976 - WNC Tax Credits 38, LLC, WNC Tax Credits 39, LLC, WNC Housing Tax Credits Manager, LLC and WNC...

Federal Register 2010, 2011, 2012, 2013, 2014

2010-04-08

... Credits 38, LLC, WNC Tax Credits 39, LLC, WNC Housing Tax Credits Manager, LLC and WNC & Associates, Inc... collectively, the ``Funds''), WNC Housing Tax Credits Manager, LLC (the ``Manager'') and WNC & Associates, Inc... credit under the Internal Revenue Code of 1986, as amended. The Manager is a California limited liability...

Toward State Tax Reform: Lessons from State Tax Studies.

ERIC Educational Resources Information Center

McGuire, Therese J.; Rio, Jessica E.

This paper reviews recent state tax-commission recommendations in selected states and identifies critical factors for the success of state tax-reform commissions. The paper focuses on factors linked to the process of forming a commission and generating the necessary consensus to enact tough reforms. It describes and compares comprehensive studies…

Asymmetric cell division requires specific mechanisms for adjusting global transcription.

PubMed

Mena, Adriana; Medina, Daniel A; García-Martínez, José; Begley, Victoria; Singh, Abhyudai; Chávez, Sebastián; Muñoz-Centeno, Mari C; Pérez-Ortín, José E

2017-12-01

Most cells divide symmetrically into two approximately identical cells. There are many examples, however, of asymmetric cell division that can generate sibling cell size differences. Whereas physical asymmetric division mechanisms and cell fate consequences have been investigated, the specific problem caused by asymmetric division at the transcription level has not yet been addressed. In symmetrically dividing cells the nascent transcription rate increases in parallel to cell volume to compensate it by keeping the actual mRNA synthesis rate constant. This cannot apply to the yeast Saccharomyces cerevisiae, where this mechanism would provoke a never-ending increasing mRNA synthesis rate in smaller daughter cells. We show here that, contrarily to other eukaryotes with symmetric division, budding yeast keeps the nascent transcription rates of its RNA polymerases constant and increases mRNA stability. This control on RNA pol II-dependent transcription rate is obtained by controlling the cellular concentration of this enzyme. © The Author(s) 2017. Published by Oxford University Press on behalf of Nucleic Acids Research.

Alcohol taxes and birth outcomes.

PubMed

Zhang, Ning

2010-05-01

This study examines the relationships between alcohol taxation, drinking during pregnancy, and infant health. Merged data from the US Natality Detailed Files, as well as the Behavioral Risk Factor Surveillance System (1985-2002), data regarding state taxes on beer, wine, and liquor, a state- and year-fixed-effect reduced-form regression were used. Results indicate that a one-cent ($0.01) increase in beer taxes decreased the incidence of low-birth-weight by about 1-2 percentage points. The binge drinking participation tax elasticity is -2.5 for beer and wine taxes and -9 for liquor taxes. These results demonstrate the potential intergenerational impact of increasing alcohol taxes.

The rgg0182 gene encodes a transcriptional regulator required for the full Streptococcus thermophilus LMG18311 thermal adaptation.

PubMed

Henry, Romain; Bruneau, Emmanuelle; Gardan, Rozenn; Bertin, Stéphane; Fleuchot, Betty; Decaris, Bernard; Leblond-Bourget, Nathalie

2011-10-07

Streptococcus thermophilus is an important starter strain for the production of yogurt and cheeses. The analysis of sequenced genomes of four strains of S. thermophilus indicates that they contain several genes of the rgg familly potentially encoding transcriptional regulators. Some of the Rgg proteins are known to be involved in bacterial stress adaptation. In this study, we demonstrated that Streptococcus thermophilus thermal stress adaptation required the rgg0182 gene which transcription depends on the culture medium and the growth temperature. This gene encoded a protein showing similarity with members of the Rgg family transcriptional regulator. Our data confirmed that Rgg0182 is a transcriptional regulator controlling the expression of its neighboring genes as well as chaperones and proteases encoding genes. Therefore, analysis of a Δrgg0182 mutant revealed that this protein played a role in the heat shock adaptation of Streptococcus thermophilus LMG18311. These data showed the importance of the Rgg0182 transcriptional regulator on the survival of S. thermophilus during dairy processes and more specifically during changes in temperature.

Tax Information Series, December 2000

DTIC Science & Technology

2001-03-14

to serve as an in-depth review or explanation of each topic discussed, rather its intent is to inform readers about updates in tax numerology and... NUMEROLOGY Tax Rates The 2000 federal income tax rates are: 15%, 28%, 31%, 36%, and 39.6%. The 2000 tax rates by filing status are

Intercollegiate Athletics Subsidies: A Regressive Tax

ERIC Educational Resources Information Center

Denhart, Matthew; Vedder, Richard

2010-01-01

For most colleges and universities in the United States, intercollegiate athletics is a losing financial proposition. The vast majority ICA departments do not break even and require subsidization from the institution as a whole. When schools are forced to heavily subsidize athletics, ICA serves to impose an "athletics tax" on other dimensions of…

7 CFR 1436.14 - Taxes.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 7 Agriculture 10 2011-01-01 2011-01-01 false Taxes. 1436.14 Section 1436.14 Agriculture... Taxes. The borrower must pay, when due, all real and personal property taxes that may affect CCC's..., CCC may pay any unpaid taxes with respect to the collateral or land securing a loan made in accordance...

7 CFR 1436.14 - Taxes.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 7 Agriculture 10 2010-01-01 2010-01-01 false Taxes. 1436.14 Section 1436.14 Agriculture... Taxes. The borrower must pay, when due, all real and personal property taxes that may affect CCC's..., CCC may pay any unpaid taxes with respect to the collateral or land securing a loan made in accordance...

Human T-Cell Leukemia Virus I Tax Protein Sensitizes p53-Mutant Cells to DNA Damage