NDLI: Identification of TRIML2, a Novel p53 Target, that Enhances p53-SUMOylation and Regulates the Transactivation of Pro-apoptotic Genes

Content Provider	PubMed Central
Author	Kung, Che-pei Khaku, Sakina Jennis, Matthew Zhou, Yan Murphy, Maureen E.
Abstract	The tumor suppressor protein p53, encoded by TP53, inhibits tumorigenesis by inducing cell cycle arrest, senescence and apoptosis. Several genetic polymorphisms exist in TP53, including a proline to arginine variant at amino acid 72 (P72 and R72, respectively); this polymorphism alters p53 function. In general, the P72 variant shows increased ability to induce cell cycle arrest, while the R72 variant possesses increased ability to induce apoptosis, relative to P72. At present, the underlying mechanisms for these functional differences are not fully understood. Toward elucidating the molecular basis for these differences a gene expression microarray analysis was conducted on normal human fibroblast cells that are homozygous for P72 and R72 variants, along with subclones of these lines that express a p53 short hairpin (shp53). Approximately three dozen genes were identified whose transactivation is affected by the codon 72 polymorphism. One of these is the tripartite motif family-like 2 (TRIML2) gene, which is preferentially induced by the R72 variant. Importantly, the accumulated data indicate that TRIML2 interacts with p53, and facilitates the modification of p53 with SUMO2. TRIML2 also enhances the ability of p53 to transactivate a subset of pro-apoptotic target genes associated with prolonged oxidative stress, including PIDD, PIG3 (TP53I3) and PIG6 (PRODH). These data indicate that TRIML2 is part of a feed-forward loop that activates p53 in cells expressing the R72 variant, particularly after prolonged stress.
Related Links	http://dx.doi.org/10.1158/1541-7786.mcr-14-0385
Ending Page	262
Page Count	13
Starting Page	250
File Format	PDF
ISSN	15417786
e-ISSN	15573125
Journal	Molecular cancer research : MCR
Issue Number	2
Volume Number	13
Language	English
Publisher Date	2015-02-01
Access Restriction	Open
Subject Keyword	Cancer Research Oncology Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Cancer Research Oncology

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1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
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