ArticleOncogene2002
Multiple lysine mutations in the C-terminus of p53 make it resistant to degradation mediated by MDM2 but not by human papillomavirus E6 and induce growth inhibition in MDM2-overexpressing cells.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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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
7 citing papers in PubMed, 18 citations in OpenAlex.
- p53 Frameshift Mutations Couple Loss-of-Function with Unique Neomorphic Activities.Molecular cancer research : MCR · 2021Article
- The p53 isoforms are differentially modified by Mdm2.Cell cycle (Georgetown, Tex.) · 2012Article
- Regulation of the nucleocytoplasmic trafficking of viral and cellular proteins by ubiquitin and small ubiquitin-related modifiers.Biology of the cell · 2012Review
- Hairless expression attenuates apoptosis in a mouse model and the COS cell line; involvement of p53.PloS one · 2010Article
- Activating transcription factor 3 activates p53 by preventing E6-associated protein from binding to E6.The Journal of biological chemistry · 2010Article
- Ubiquitin-independent degradation of p53 mediated by high-risk human papillomavirus protein E6.Oncogene · 2007Article
- The CBP/p300 TAZ1 domain in its native state is not a binding partner of MDM2.The Biochemical journal · 2004Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We have recently shown that lysine mutations in p53's putative C-terminal acetylation sites result in increased stability and cytoplasmic distribution of the p53 protein in a human lung cancer cell line. In the present study, we showed that when lysine residues 372, 373, 381, and 382 of p53 were substituted with alanine, the resulting A4 protein was resistant to MDM2-mediated proteosomal degradation but was highly sensitive to human papillomavirus E6-mediated proteolysis. When A4 and wild-type p53 were transfected into MDM2-overexpressing MCF-7 cells, A4 significantly reduced colony formation in vitro, when compared with wild-type p53. Our results suggest that A4 exerts a growth-inhibitory effect more efficiently than wild-type p53 does in cell lines that overexpress MDM2 and may therefore be a better therapeutic tool than wild-type p53 for certain cancers in which MDM2 is amplified or overexpressed.
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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.