ArticleJournal of virology2008
Human T-cell leukemia virus type 1 tax attenuates the ATM-mediated cellular DNA damage response.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 51 citations in OpenAlex.
- Systems biology approaches reveal a specific interferon-inducible signature in HTLV-1 associated myelopathy.PLoS pathogens · 2012Trial
- Review
- Review
- HTLV-1 Tax Tug-of-War: Cellular Senescence and Death or Cellular Transformation.Pathogens (Basel, Switzerland) · 2024Review
- Dynamics and consequences of the HTLV-1 proviral plus-strand burst.PLoS pathogens · 2022Article
- Regulation of HTLV-1 transformation.Bioscience reports · 2022Review
- Adult T-cell leukemia-lymphoma as a viral disease: Subtypes based on viral aspects.Cancer science · 2021Review
- Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020Review
- The Human T-Cell Leukemia Virus Type 1 Basic Leucine Zipper Factor Attenuates Repair of Double-Stranded DNA Breaks via Nonhomologous End Joining.Journal of virology · 2018Article
- DNA Damage Response Signals Transduce Stress From Rheumatoid Arthritis Risk Factors Into T Cell Dysfunction.Frontiers in immunology · 2018Review
- Potential of Radiation-Induced Cellular Stress for Reactivation of Latent HIV-1 and Killing of Infected Cells.AIDS research and human retroviruses · 2016Article
- Activation of the DNA Damage Response by RNA Viruses.Biomolecules · 2016Review
- HTLV-I Tax-Mediated Inactivation of Cell Cycle Checkpoints and DNA Repair Pathways Contribute to Cellular Transformation: "A Random Mutagenesis Model".Journal of cancer sciences · 2015Article
- Modes of Human T Cell Leukemia Virus Type 1 Transmission, Replication and Persistence.Viruses · 2015Review
- Review
- Tumor Suppressor Inactivation in the Pathogenesis of Adult T-Cell Leukemia.Journal of oncology · 2015Review
- Human viruses and cancer.Viruses · 2014Review
- Human T-lymphotropic virus type 1-infected cells secrete exosomes that contain Tax protein.The Journal of biological chemistry · 2014Article
- The DNA damage response induced by infection with human cytomegalovirus and other viruses.Viruses · 2014Review
- Acetylation at lysine 346 controls the transforming activity of the HTLV-1 Tax oncoprotein in the Rat-1 fibroblast model.Retrovirology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Genomic instability, a hallmark of leukemic cells, is associated with malfunctioning cellular responses to DNA damage caused by defective cell cycle checkpoints and/or DNA repair. Adult T-cell leukemia, which can result from infection with human T-cell leukemia virus type 1 (HTLV-1), is associated with extensive genomic instability that has been attributed to the viral oncoprotein Tax. How Tax influences cellular responses to DNA damage to mediate genomic instability, however, remains unclear. Therefore, we investigated the effect of Tax on cellular pathways involved in recognition and repair of DNA double-strand breaks. Premature attenuation of ATM kinase activity and reduced association of MDC1 with repair foci were observed in Tax-expressing cells. Following ionizing radiation-induced S-phase checkpoint activation, Tax-expressing cells progressed more rapidly than non-Tax-expressing cells toward DNA replication. These results demonstrate that Tax expression may allow premature DNA replication in the presence of genomic lesions. Attempts to replicate in the presence of these lesions would result in gradual accumulation of mutations, leading to genome instability and cellular transformation.
Indexed as
Identifiers
What OpenQuestion holds
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.