ArticleJournal of virology1997
Human T-cell leukemia virus type 1 Tax releases cell cycle arrest induced by p16INK4a.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 130 citations in OpenAlex.
- Review
- Review
- Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020Review
- Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018Review
- Cell cycle regulation during viral infection.Methods in molecular biology (Clifton, N.J.) · 2014Review
- Activation of WIP1 phosphatase by HTLV-1 Tax mitigates the cellular response to DNA damage.PloS one · 2013Article
- Development of ultra-super sensitive immunohistochemistry and its application to the etiological study of adult T-cell leukemia/lymphoma.Acta histochemica et cytochemica · 2012Article
- The human T-cell leukemia virus type 1 oncoprotein tax controls forkhead box O4 activity through degradation by the proteasome.Journal of virology · 2011Article
- Human T-cell leukemia virus type 1 (HTLV-1) and leukemic transformation: viral infectivity, Tax, HBZ and therapy.Oncogene · 2011Review
- Complex cell cycle abnormalities caused by human T-lymphotropic virus type 1 Tax.Journal of virology · 2011Article
- Article
- Human T-lymphotropic virus type 1 transcription and chromatin-remodeling complexes.Journal of virology · 2010Article
- Distinct functions of HTLV-1 Tax1 from HTLV-2 Tax2 contribute key roles to viral pathogenesis.Retrovirology · 2009Review
- The HTLV-1 Tax interactome.Retrovirology · 2008Review
- Effect of transforming viruses on molecular mechanisms associated with cancer.Journal of cellular physiology · 2008Review
- Two specific drugs, BMS-345541 and purvalanol A induce apoptosis of HTLV-1 infected cells through inhibition of the NF-kappaB and cell cycle pathways.AIDS research and therapy · 2008Article
- Role of human T-cell leukemia virus type I Tax in expression of the human telomerase reverse transcriptase (hTERT) gene in human T-cells.Cancer science · 2008Article
- Viruses associated with human cancer.Biochimica et biophysica acta · 2008Review
- HTLV-1 propels untransformed CD4 lymphocytes into the cell cycle while protecting CD8 cells from death.The Journal of clinical investigation · 2006Article
- The HTLV-1 Tax protein binding domain of cyclin-dependent kinase 4 (CDK4) includes the regulatory PSTAIRE helix.Retrovirology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein causes cellular transformation by deregulating important cellular processes such as DNA repair, transcription, signal transduction, proliferation, and growth. Although it is clear that normal cell cycle control is deregulated during HTLV-1-induced cellular transformation, the effects of Tax on cell cycle control are not well understood. Flow cytometric analyses of human T cells indicate that cell cycle arrest in late G1, at or before the G1/S restriction point, by p16INK4a is relieved by Tax. Furthermore, Tax-dependent stimulation of 5-bromo-2'-deoxyuridine incorporation and transcriptional activation is inhibited by p16INK4a. This result suggests that p16INK4a is able to block Tax-dependent stimulation of DNA synthesis and cell cycle progression into S phase. In vitro binding assays with recombinant glutathione S-transferase fusion proteins and [35S]methionine-labeled proteins indicate that Tax binds specifically with p16INK4a but not with either p21cip1 or p27kip1. Furthermore, sequential immunoprecipitation assays with specific antisera and [35S]methionine-labeled cell lysates subsequent to coexpression with Tax and p16INK4a indicate that the two proteins form complexes in vivo. Immunocomplex kinase assays with cyclin-dependent kinase 4 antiserum indicate that Tax blocks the inhibition of cdk4 kinase activity by p16INK4a. This study identifies p16INK4a as a novel cellular target for Tax and suggests that the inactivation of p16INK4a function is a mechanism of cell cycle deregulation by Tax.
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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.