ArticleOncogene2005
High levels of cytoplasmic HTLV-1 Tax mutant proteins retain a Tax-NF-kappaB-CBP ternary complex in the cytoplasm.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Molecular Studies of HTLV-1 Replication: An Update.Viruses · 2016Review
- 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
- Animal models on HTLV-1 and related viruses: what did we learn?Frontiers in microbiology · 2012Article
- Cotranscriptional Chromatin Remodeling by Small RNA Species: An HTLV-1 Perspective.Leukemia research and treatment · 2012Article
- Article
- p53 Oligomerization is essential for its C-terminal lysine acetylation.The Journal of biological chemistry · 2009Article
- The HTLV-1 Tax interactome.Retrovirology · 2008Review
- Dengue virus replicon expressing the nonstructural proteins suffices to enhance membrane expression of HLA class I and inhibit lysis by human NK cells.Journal of virology · 2008Article
- HTLV-1 tax-induced NF-kappaB activation is synergistically enhanced by 12-O-tetradecanoylphorbol-13-acetate: mechanism and implications for Tax oncogenicity.Journal of molecular medicine (Berlin, Germany) · 2008Article
- Ubiquitination of HTLV-I Tax in response to DNA damage regulates nuclear complex formation and nuclear export.Retrovirology · 2007Article
- Article
- Modulation of dendritic cell maturation and function by the Tax protein of human T cell leukemia virus type 1.Journal of leukocyte biology · 2007Article
- Suppression of viral gene expression in bovine leukemia virus-associated B-cell malignancy: interplay of epigenetic modifications leading to chromatin with a repressive histone code.Journal of virology · 2007Article
- Interaction of HTLV-1 Tax protein with calreticulin: implications for Tax nuclear export and secretion.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2007Article
- Manipulation of the nuclear factor-kappaB pathway and the innate immune response by viruses.Oncogene · 2006Review
- Genotoxic stress and cellular stress alter the subcellular distribution of human T-cell leukemia virus type 1 tax through a CRM1-dependent mechanism.Journal of virology · 2006Article
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The oncogenic potential of HTLV-1 Tax protein is partially ascribed to its capacity to activate NF-kappaB. The current view is that Tax acts first in the cytoplasm to dissociate NF-kappaB factors from the IkappaB proteins and enable their nuclear translocation, then Tax links p65(RelA), within the nucleus, to CBP/p300 and P/CAF, which are essential for its optimal transcriptional activity. Our present study challenges the paradigm that Tax-p65(RelA)-CBP/p300 assembly occurs in the nucleus. Using Tax mutants defective for nuclear localization we show that at low levels these mutants induce the nuclear translocation of NF-kappaB factors but not their transcriptional activity, whereas at high levels they trap CBP and free p65(RelA) in the cytoplasm and block, thereby, their transcriptional function. In contrast, wild-type (w.t.) Tax strongly stimulated NF-kappaB-dependent gene expression in all tested experimental settings. These data suggest that the Tax-p65(RelA)-CBP ternary complex is established in the cytoplasm rather than in the nucleus. When this complex is formed with w.t. Tax, the entire moiety translocates into the nucleus and exerts high transcriptional activity. However, if the complex is formed with the cytoplasmic Tax mutants, the resulting moiety is retained in the cytoplasm and is, therefore, devoid of transcriptional activity.
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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.