ArticleJournal of virology2006
Genotoxic stress and cellular stress alter the subcellular distribution of human T-cell leukemia virus type 1 tax through a CRM1-dependent mechanism.
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 19 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020Review
- Article
- The Major Histocompatibility Complex Class II Transactivator CIITA Inhibits the Persistent Activation of NF-κB by the Human T Cell Lymphotropic Virus Type 1 Tax-1 Oncoprotein.Journal of virology · 2016Article
- Regulation of HTLV-1 tax stability, cellular trafficking and NF-κB activation by the ubiquitin-proteasome pathway.Viruses · 2014Review
- The four and a half LIM family members are novel interactants of the human T-cell leukemia virus type 1 Tax oncoprotein.Journal of virology · 2013Article
- Tax-1 and Tax-2 similarities and differences: focus on post-translational modifications and NF-κB activation.Frontiers in microbiology · 2013Article
- An RNA interference screen identifies the Deubiquitinase STAMBPL1 as a critical regulator of human T-cell leukemia virus type 1 tax nuclear export and NF-κB activation.Journal of virology · 2012Article
- Regulation of the nucleocytoplasmic trafficking of viral and cellular proteins by ubiquitin and small ubiquitin-related modifiers.Biology of the cell · 2012Review
- Article
- Animal models on HTLV-1 and related viruses: what did we learn?Frontiers in microbiology · 2012Article
- The HTLV-1 Tax protein inhibits formation of stress granules by interacting with histone deacetylase 6.Oncogene · 2011Article
- Review
- Move or die: the fate of the Tax oncoprotein of HTLV-1.Viruses · 2011Review
- Viral oncogenes, noncoding RNAs, and RNA splicing in human tumor viruses.International journal of biological sciences · 2010Review
- Role of post-translational modifications of HTLV-1 Tax in NF-κB activation.World journal of biological chemistry · 2010Article
- Human T-cell leukemia virus type 1 Tax relieves repression of proliferating cell nuclear antigen gene expression.Journal of virology · 2008Article
- The HTLV-1 Tax interactome.Retrovirology · 2008Review
- Human T-cell leukemia virus type 1 tax attenuates the ATM-mediated cellular DNA damage response.Journal of virology · 2008Article
- Ubiquitination of HTLV-I Tax in response to DNA damage regulates nuclear complex formation and nuclear export.Retrovirology · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Human T-cell leukemia virus type 1 Tax is a predominantly nuclear viral oncoprotein that colocalizes with cellular proteins in nuclear foci known as Tax speckled structures (TSS). Tax is also diffusely distributed throughout the cytoplasm, where it interacts with and affects the functions of cytoplasmic cellular proteins. Mechanisms that regulate the distribution of Tax between the cytoplasm and nucleus remain to be identified. Since Tax has been shown to promote genome instability by perturbing cell cycle progression and DNA repair mechanisms following DNA damage, we examined the effect of genotoxic stress on the subcellular distribution and interacting partners of Tax. Tax localization was altered in response to various forms of cellular stress, resulting in an increase in cytoplasmic Tax and a decrease in Tax speckled structures. Concomitantly, colocalization of Tax with sc35 (a TSS protein) decreased following stress. Tax translocation required the CRM1 nuclear export pathway, and a transient interaction between Tax and CRM1 was observed following stress. These results suggest that the subcellular distribution of Tax and the interactions between Tax and cellular proteins respond dynamically to cellular stress. Changes in Tax distribution and interacting partners are likely to affect cellular processes that regulate cellular transformation.
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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.