ArticleJournal of virology2006
Versatile reporter systems show that transactivation by human T-cell leukemia virus type 1 Tax occurs independently of chromatin remodeling factor BRG1.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Development of a CRE/CREB-driven HBx responsive HBV cell culture reporter system for antiviral drug evaluation.JHEP reports : innovation in hepatology · 2025Article
- A Novel Tax-Responsive Reporter T-Cell Line to Analyze Infection of HTLV-1.Pathogens (Basel, Switzerland) · 2024Article
- Dynamics and consequences of the HTLV-1 proviral plus-strand burst.PLoS pathogens · 2022Article
- Time-course of host cell transcription during the HTLV-1 transcriptional burst.PLoS pathogens · 2022Article
- Epigenetic Regulation of Human T-Cell Leukemia Virus Gene Expression.Microorganisms · 2021Review
- NF-κB-induced R-loop accumulation and DNA damage select for nucleotide excision repair deficiencies in adult T cell leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Novel Interactions between the Human T-Cell Leukemia Virus Type 1 Antisense Protein HBZ and the SWI/SNF Chromatin Remodeling Family: Implications for Viral Life Cycle.Journal of virology · 2019Article
- Cells of adult T-cell leukemia evade HTLV-1 Tax/NF-κB hyperactivation-induced senescence.Blood advances · 2019Article
- Sporadic on/off switching of HTLV-1 Tax expression is crucial to maintain the whole population of virus-induced leukemic cells.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- HTLV-1 Tax Stimulates Ubiquitin E3 Ligase, Ring Finger Protein 8, to Assemble Lysine 63-Linked Polyubiquitin Chains for TAK1 and IKK Activation.PLoS pathogens · 2015Article
- KSHV vCyclin counters the senescence/G1 arrest response triggered by NF-κB hyperactivation.Oncogene · 2015Article
- Regulation of human T-lymphotropic virus type I latency and reactivation by HBZ and Rex.PLoS pathogens · 2014Article
- NF-κB inhibition facilitates the establishment of cell lines that chronically produce human T-lymphotropic virus type 1 viral particles.Journal of virology · 2014Article
- 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.Frontiers in microbiology · 2013Article
- HTLV-1 tax-induced rapid senescence is driven by the transcriptional activity of NF-κB and depends on chronically activated IKKα and p65/RelA.Journal of virology · 2012Article
- NF-κB hyper-activation by HTLV-1 tax induces cellular senescence, but can be alleviated by the viral anti-sense protein HBZ.PLoS pathogens · 2011Article
- Complex cell cycle abnormalities caused by human T-lymphotropic virus type 1 Tax.Journal of virology · 2011Article
- Human T-lymphotropic virus type 1 transcription and chromatin-remodeling complexes.Journal of virology · 2010Article
- Induction of p21(CIP1/WAF1) expression by human T-lymphotropic virus type 1 Tax requires transcriptional activation and mRNA stabilization.Retrovirology · 2009Article
- Human T-cell leukemia virus type 1 infection leads to arrest in the G1 phase of the cell cycle.Journal of virology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Potent activation of human T-cell leukemia virus type 1 (HTLV-1) gene expression is mediated by the virus-encoded transactivator protein Tax and three imperfect 21-bp repeats in the viral long terminal repeats. Each 21-bp repeat contains a cAMP-responsive-element core flanked by 5' G-rich and 3' C-rich sequences. Tax alone does not bind DNA. Rather, it interacts with basic domain-leucine zipper transcription factors CREB and ATF-1 to form ternary complexes with the 21-bp repeats. In the context of the ternary complexes, Tax contacts the G/C-rich sequences and recruits transcriptional coactivators CREB-binding protein (CBP)/p300 to effect potent transcriptional activation. Using an easily transduced and chromosomally integrated reporter system derived from a self-inactivating lentivirus vector, we showed in a BRG1- and BRM1-deficient adrenal carcinoma cell line, SW-13, that Tax- and 21-bp repeat-mediated transactivation does not require BRG1 or BRM1 and is not enhanced by BRG1. With a similar reporter system, we further demonstrated that Tax- and tumor necrosis factor alpha-induced NF-kappaB activation occurs readily in SW-13 cells in the absence of BRG1 and BRM1. These results suggest that the assembly of stable multiprotein complexes containing Tax, CREB/ATF-1, and CBP/p300 on the 21-bp repeats is the principal mechanism employed by Tax to preclude nucleosome formation at the HTLV-1 enhancer/promoter. This most likely bypasses the need for BRG1-containing chromatin-remodeling complexes. Likewise, recruitment of CBP/p300 by NF-kappaB may be sufficient to disrupt histone-DNA interaction for the initiation of transcription.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.