ArticleMolecular and cellular biology2004
Transcription regulatory complexes bind the human T-cell leukemia virus 5' and 3' long terminal repeats to control gene expression.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 61 citations in OpenAlex.
- Prevalence and genetic diversity of HTLV-1 among blood donors in Jiroft, Iran: a comprehensive study.Virus genes · 2025Article
- Upregulation of Neuropilin-1 Inhibits HTLV-1 Infection.Pathogens (Basel, Switzerland) · 2023Article
- HBZ upregulates myoferlin expression to facilitate HTLV-1 infection.PLoS pathogens · 2023Article
- Regulation of human T-cell leukemia virus type 1 antisense promoter by myocyte enhancer factor-2C in the context of adult T-cell leukemia and lymphoma.Haematologica · 2022Article
- Novel perspectives on antisense transcription in HIV-1, HTLV-1, and HTLV-2.Frontiers in microbiology · 2022Review
- HDAC inhibitors Panobinostat and Romidepsin enhanceFrontiers in immunology · 2022Article
- Latency Reversing Agents: Kick and Kill of HTLV-1?International journal of molecular sciences · 2021Review
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- Epigenetic changes around the pX region and spontaneous HTLV-1 transcription are CTCF-independent.Wellcome open research · 2018Article
- RNA stability regulates human T cell leukemia virus type 1 gene expression in chronically-infected CD4 T cells.Virology · 2017Article
- The sense behind retroviral anti-sense transcription.Virology journal · 2017Article
- Review
- Review
- Characteristics of Adult T-Cell Leukemia/Lymphoma Patients with Long Survival: Prognostic Significance of Skin Lesions and Possible Beneficial Role of Valproic Acid.Leukemia research and treatment · 2015Article
- HBZ stimulates brain-derived neurotrophic factor/TrkB autocrine/paracrine signaling to promote survival of human T-cell leukemia virus type 1-Infected T cells.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
- The HTLV-1-encoded protein HBZ directly inhibits the acetyl transferase activity of p300/CBP.Nucleic acids research · 2012Article
- Nuclear export and expression of human T-cell leukemia virus type 1 tax/rex mRNA are RxRE/Rex dependent.Journal of virology · 2012Article
- HTLV tax: a fascinating multifunctional co-regulator of viral and cellular pathways.Frontiers in microbiology · 2012Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that integrates randomly into the T-cell genome. Two long terminal repeats (LTRs) flank the integrated provirus. The upstream and downstream LTRs carry identical promoter sequences. Studies with other retroviruses suggest that the downstream promoter is silent and that RNA polymerases initiating at the upstream promoter proceed through the 3' LTR. In this study, we used the chromatin immunoprecipitation assay to compare the binding of transcription regulatory proteins at both the upstream and downstream promoters in HTLV-1-infected cell lines and adult T-cell leukemia-lymphoma cells. Unexpectedly, we detected a nearly equal distribution of activator (Tax, CREB, ATF-1, ATF-2, c-Fos, and c-Jun) and regulatory protein (CBP, p300, TAF(II)250, and polymerase II) binding at both the upstream and downstream promoters. Consistent with this observation, we found that the downstream promoter was transcriptionally active, suggesting that the two promoters are functionally equivalent. We also detected asymmetrical binding of histone deacetylases (HDAC-1, -2, and -3) at both promoters. All three HDACs strongly repressed Tax transactivation, and this repression correlated with displacement of Tax from the HTLV-1 promoter. These effects were reciprocal, as Tax expression reversed HDAC repression and displaced HDACs from the HTLV-1 promoter. These data suggest that HTLV-1 transcriptional regulation at both the 5' and 3' LTRs is mediated, in part, through the mutually exclusive binding of Tax and HDACs at the proviral promoters.
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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.