ArticleJournal of virology2000
pRB-dependent, J domain-independent function of simian virus 40 large T antigen in override of p53 growth suppression.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Hepatocyte Models for Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comparative Analysis of Non-HepG2 Cell Models.International journal of molecular sciences · 2026Review
- The Microbial Metabolite IDA Sensitizes Tumor Cells to ARF1 Inhibition by Inducing SVIL-dependent Senescence.International journal of biological sciences · 2026Article
- J domain independent functions of J proteins.Cell stress & chaperones · 2016Review
- T antigen transformation reveals Tp53/RB-dependent route to PLAC1 transcription activation in primary fibroblasts.Oncogenesis · 2013Article
- Article
- A feedback loop involving the Phd3 prolyl hydroxylase tunes the mammalian hypoxic response in vivo.Molecular and cellular biology · 2009Article
- Somatic inactivation of the PHD2 prolyl hydroxylase causes polycythemia and congestive heart failure.Blood · 2008Article
- Truncated N-terminal mutants of SV40 large T antigen as minimal immortalizing agents for CNS cells.Experimental neurology · 2005Article
- Simian virus 40 large T antigen targets the spindle assembly checkpoint protein Bub1.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Heat-shock proteins as regulators of apoptosis.Oncogene · 2003Review
- Negative regulation of mitotic promoting factor by the checkpoint kinase chk1 in simian virus 40 lytic infection.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
- Cell density related gene expression: SV40 large T antigen levels in immortalized astrocyte lines.BMC cell biology · 2002Article
- Enumeration of the simian virus 40 early region elements necessary for human cell transformation.Molecular and cellular biology · 2002Article
- 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
- Loss of p16 pathways stabilizes EWS/FLI1 expression and complements EWS/FLI1 mediated transformation.Oncogene · 2001Article
- Induction of p53-independent apoptosis by simian virus 40 small t antigen.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
- J domain-independent regulation of the Rb family by polyomavirus large T antigen.Journal of virology · 2000Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Simian virus 40 (SV40) large T antigen (LT) can immortalize and transform many cell types. These activities are attributed in large part to the binding and functional inactivation by LT of two major tumor suppressors: p53 and the retinoblastoma protein, pRB. Most effects of LT on pRB have been shown to additionally require an intact J domain, which mediates binding to Hsc70. We show here that the J domain is not required for p53 override in full-length LT. Although LT binds p53, it was shown previously that overcoming a p53-induced cell cycle arrest requires binding to pRB family members (R. S. Quartin et al., J. Virol. 68:1334-1341). We demonstrate that an LT mutant defective for pRB family member binding (K1) can be complemented for efficient override of p53 arrest by a construct encoding the first 135 amino acids of LT with a J domain-inactivating mutation, H42Q. Hence, complementation does not require the J domain, and pRB binding by LT is important for more than dissociating pRB-E2F complexes, which is J dependent. In accordance with this notion, LT alleviates pRB small-pocket-mediated transcriptional repression independently of the J domain. The LT K1 mutant can also be complemented for p53 override by small t antigen (st) in a manner independent of its J domain. Our observations underscore the importance of multiple SV40 functions, two in LT and one in st, that act cooperatively to counteract p53 growth suppression.
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