ArticleMolecular and cellular biology1998
The J domain of simian virus 40 large T antigen is required to functionally inactivate RB family proteins.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 149 citations in OpenAlex.
- Merkel cell polyomavirus T-antigens regulateiScience · 2021Article
- Stress proteins: the biological functions in virus infection, present and challenges for target-based antiviral drug development.Signal transduction and targeted therapy · 2020Review
- Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018Review
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- RB1 is the crucial target of the Merkel cell polyomavirus Large T antigen in Merkel cell carcinoma cells.Oncotarget · 2016Article
- A Strategy for Direct Chemical Activation of the Retinoblastoma Protein.ACS chemical biology · 2016Article
- The conserved core enzymatic activities and the distinct dynamics of polyomavirus large T antigens.Archives of biochemistry and biophysics · 2015Article
- Sestrin 2 protein regulates platelet-derived growth factor receptor β (Pdgfrβ) expression by modulating proteasomal and Nrf2 transcription factor functions.The Journal of biological chemistry · 2015Article
- Kaposi's sarcoma-associated herpesvirus lana2 protein interacts with the pocket proteins and inhibits their sumoylation.Oncogene · 2014Article
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- Cell cycle regulation during viral infection.Methods in molecular biology (Clifton, N.J.) · 2014Review
- The HSP70 modulator MAL3-101 inhibits Merkel cell carcinoma.PloS one · 2014Article
- Inhibition of post-transcriptional RNA processing by CDK inhibitors and its implication in anti-viral therapy.PloS one · 2014Article
- T antigen transformation reveals Tp53/RB-dependent route to PLAC1 transcription activation in primary fibroblasts.Oncogenesis · 2013Article
- Binding to retinoblastoma pocket domain does not alter the inter-domain flexibility of the J domain of SV40 large T antigen.Archives of biochemistry and biophysics · 2012Article
- Article
- Cross-talk between T-Ag presence and pRb family and p53/p73 signaling in mouse and human medulloblastoma.Journal of cellular biochemistry · 2010Article
- Id2 deficiency promotes metastasis in a mouse model of ocular cancer.Clinical & experimental metastasis · 2010Article
- Simian virus 40 T-antigen-mediated gene regulation in enterocytes is controlled primarily by the Rb-E2F pathway.Journal of virology · 2009Article
- Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Transformation by simian virus 40 large T antigen (TAg) is dependent on the inactivation of cellular tumor suppressors. Transformation minimally requires the following three domains: (i) a C-terminal domain that mediates binding to p53; (ii) the LXCXE domain (residues 103 to 107), necessary for binding to the retinoblastoma tumor suppressor protein, pRB, and the related p107 and p130; and (iii) an N-terminal domain that is homologous to the J domain of DnaJ molecular chaperone proteins. We have previously demonstrated that the N-terminal J domain of TAg affects the RB-related proteins by perturbing the phosphorylation status of p107 and p130 and promoting the degradation of p130 and that this domain is required for transformation of cells that express either p107 or p130. In this work, we demonstrate that the J domain of TAg is required to inactivate the ability of each member of the pRB family to induce a G1 arrest in Saos-2 cells. Furthermore, the J domain is required to override the repression of E2F activity mediated by p130 and pRB and to disrupt p130-E2F DNA binding complexes. These results imply that while the LXCXE domain serves as a binding site for the RB-related proteins, the J domain plays an important role in inactivating their function.
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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.