ArticleJournal of virology2005
Intestinal dysplasia induced by simian virus 40 T antigen is independent of p53.
Article in Journal of virology, 2005. 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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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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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Expression of the small T antigen of Lymphotropic Papovavirus is sufficient to transform primary mouse embryo fibroblasts.Virology · 2016Article
- Polyomavirus T antigens activate an antiviral state.Virology · 2015Article
- Removal of a small C-terminal region of JCV and SV40 large T antigens has differential effects on transformation.Virology · 2014Article
- Viral oncogene expression in the stem/progenitor cell compartment of the mouse intestine induces adenomatous polyps.Molecular cancer research : MCR · 2014Article
- A retinoblastoma allele that is mutated at its common E2F interaction site inhibits cell proliferation in gene-targeted mice.Molecular and cellular biology · 2014Article
- Two independent regions of simian virus 40 T antigen increase CBP/p300 levels, alter patterns of cellular histone acetylation, and immortalize primary cells.Journal of virology · 2013Article
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- Prevention of senescence progression in reversibly immortalized human ensheathing glia permits their survival after deimmortalization.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Article
- Simian virus 40 T-antigen-mediated gene regulation in enterocytes is controlled primarily by the Rb-E2F pathway.Journal of virology · 2009Article
- T antigen transgenic mouse models.Seminars in cancer biology · 2009Review
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- Intestinal hyperplasia induced by simian virus 40 large tumor antigen requires E2F2.Journal of virology · 2007Article
- Enterocyte proliferation and intestinal hyperplasia induced by simian virus 40 T antigen require a functional J domain.Journal of virology · 2007Article
- SV40 large T antigen targets multiple cellular pathways to elicit cellular transformation.Oncogene · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Transgenic mice expressing simian virus 40 large T antigen in enterocytes develop intestinal hyperplasia that progresses to dysplasia with age. Hyperplasia is dependent on T antigen binding to the retinoblastoma (pRb) family of tumor suppressor proteins. Mice expressing a truncated T antigen that inactivates the pRb-family, but is defective for binding p53, exhibit hyperplasia but do not progress to dysplasia. We hypothesized that the inhibition of the pRb family leads to entry of enterocytes into the cell cycle, resulting in hyperplasia, while inactivation of p53 is required for progression to dysplasia. Therefore, we examined T antigen/p53 complexes from the intestines of transgenic mice. We found that T antigen did not induce p53 stabilization, and we could not detect T antigen/p53 complexes in villus enterocytes. In contrast, T antigen expression led to a large increase in the levels of the cyclin-dependent kinase inhibitor p21. Furthermore, mice in which pRb was inactivated by a truncated T antigen in a p53 null background exhibited intestinal hyperplasia but no progression to dysplasia. These data indicate that loss of p53 function does not play a role in T antigen-induced dysplasia in the intestine. Rather, some unknown function of T antigen is essential for progression beyond hyperplasia.
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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.