ArticleRetrovirology2008
Human T Lymphotropic Virus Type 1 protein Tax reduces histone levels.
Article in Retrovirology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Contribution of histone variants to aneuploidy: a cancer perspective.Frontiers in genetics · 2023Pooled it
- HTLV-1-infected cells drive the differentiation of monocytes into macrophages in vitro.BMC immunology · 2025Article
- Protein Profile of Blood Monocytes is Altered in HTLV-1 Infected Patients: Implications for HAM/TSP Disease.Scientific reports · 2018Article
- Histone availability as a strategy to control gene expression.RNA biology · 2017Review
- Review
- Review
- Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer.Infectious agents and cancer · 2014Review
- Towards incorporating epigenetic mechanisms into carcinogen identification and evaluation.Carcinogenesis · 2013Review
- Autoimmunity and infection in Sjögren's syndrome.Current opinion in rheumatology · 2013Review
- Global analysis reveals multiple pathways for unique regulation of mRNA decay in induced pluripotent stem cells.Genome research · 2012Article
- Complex role of microRNAs in HTLV-1 infections.Frontiers in genetics · 2012Article
- Article
- Cotranscriptional Chromatin Remodeling by Small RNA Species: An HTLV-1 Perspective.Leukemia research and treatment · 2012Article
- HTLV tax: a fascinating multifunctional co-regulator of viral and cellular pathways.Frontiers in microbiology · 2012Article
- Distinct functions of HTLV-1 Tax1 from HTLV-2 Tax2 contribute key roles to viral pathogenesis.Retrovirology · 2009Review
- Involvement of TORC2, a CREB co-activator, in the in vivo-specific transcriptional control of HTLV-1.Retrovirology · 2009Article
- Article
- Knockdown of SLBP results in nuclear retention of histone mRNA.RNA (New York, N.Y.) · 2009Article
- The HTLV-1 Tax interactome.Retrovirology · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman T-Lymphotropic Virus Type-1 (HTLV-1) is an oncogenic retrovirus that causes adult T-cell leukemia/lymphoma (ATLL). The virally encoded Tax protein is thought to be necessary and sufficient for T-cell leukemogenesis. Tax promotes inappropriate cellular proliferation, represses multiple DNA repair mechanisms, deregulates cell cycle checkpoints, and induces genomic instability. All of these Tax effects are thought to cooperate in the development of ATLL.
resultsIn this study, we demonstrate that histone protein levels are reduced in HTLV-1 infected T-cell lines (HuT102, SLB-1 and C81) relative to uninfected T-cell lines (CEM, Jurkat and Molt4), while the relative amount of DNA per haploid complement is unaffected. In addition, we show that replication-dependent core and linker histone transcript levels are reduced in HTLV-1 infected T-cell lines. Furthermore, we show that Tax expression in Jurkat cells is sufficient for reduction of replication-dependent histone transcript levels.
conclusionThese results demonstrate that Tax disrupts the proper regulation of replication-dependent histone gene expression. Further, our findings suggest that HTLV-1 infection uncouples replication-dependent histone gene expression and DNA replication, allowing the depletion of histone proteins with cell division. Histone proteins are involved in the regulation of all metabolic processes involving DNA including transcription, replication, repair and recombination. This study provides a previously unidentified mechanism by which Tax may directly induce chromosomal instability and deregulate gene expression through reduced histone levels.
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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.