ArticleJournal of virology2000
J domain-independent regulation of the Rb family by polyomavirus large T antigen.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Stress proteins: the biological functions in virus infection, present and challenges for target-based antiviral drug development.Signal transduction and targeted therapy · 2020Review
- J domain independent functions of J proteins.Cell stress & chaperones · 2016Review
- Global Analysis of Mouse Polyomavirus Infection Reveals Dynamic Regulation of Viral and Host Gene Expression and Promiscuous Viral RNA Editing.PLoS pathogens · 2015Article
- Viral interference with DNA repair by targeting of the single-stranded DNA binding protein RPA.PLoS pathogens · 2013Article
- Comparisons between murine polyomavirus and Simian virus 40 show significant differences in small T antigen function.Journal of virology · 2011Article
- Genetic analysis of the polyomavirus DnaJ domain.Journal of virology · 2005Article
- Intestinal dysplasia induced by simian virus 40 T antigen is independent of p53.Journal of virology · 2005Article
- Activation of CREB/ATF sites by polyomavirus large T antigen.Journal of virology · 2005Article
- Simian virus 40 T antigens and J domains: analysis of Hsp40 cochaperone functions in Escherichia coli.Journal of virology · 2003Article
- Simian virus 40 large T antigen and two independent T-antigen segments sensitize cells to apoptosis following genotoxic damage.Journal of virology · 2002Article
- T antigens of simian virus 40: molecular chaperones for viral replication and tumorigenesis.Microbiology and molecular biology reviews : MMBR · 2002Review
- Regions and activities of simian virus 40 T antigen that cooperate with an activated ras oncogene in transforming primary rat embryo fibroblasts.Journal of virology · 2002Article
- Induction of p53-independent apoptosis by simian virus 40 small t antigen.Journal of virology · 2001Article
- Transactivation of murine cyclin A by polyomavirus large and small T antigens.Journal of virology · 2001Article
- Effect on polyomavirus T-antigen function of mutations in a conserved leucine-rich segment of the DnaJ domain.Journal of virology · 2001Article
- Loss of p19(ARF) eliminates the requirement for the pRB-binding motif in simian virus 40 large T antigen-mediated transformation.Molecular and cellular biology · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The ability of polyomavirus large T antigen (LT) to promote cell cycling, to immortalize primary cells, and to block differentiation has been linked to its effects on tumor suppressors of the retinoblastoma susceptibility (Rb) gene family. Our previous studies have shown that LT requires an intact N-terminal DnaJ domain, in addition to an Rb binding site, for activation of simple E2F-containing promoters and stimulation of cell cycle progression. Here we show that some LT effects dependent on interaction with the Rb family are largely DnaJ independent. In differentiating C2C12 myoblasts, overexpression of LT caused apoptosis. Although this activity of LT completely depended on Rb binding, LTs with mutations in the J domain remained able to kill. Comparisons of Rb(-) and J(-) LTs revealed additional differences. Wild-type but not Rb(-) LT activated the cyclin A promoter under serum starvation conditions. Genetic analysis of the promoter linked the Rb requirement to an E2F site in the promoter. LTs with mutations in the J domain were still able to activate the promoter. Finally, J mutant LTs caused changes in phosphorylation of both pRb and p130. In the case of p130, Thr-986 was shown to be a site that is regulated by J mutant LT. Taken together, these observations reveal that LT regulation of Rb function can be separated into both DnaJ-dependent and DnaJ-independent pathways.
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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.