Redox Modulation of p53: Mechanisms and Functional Significance

被引：44

作者：

Kim, Do-Hee ^{[1
]}

Kundu, Joydeb Kumar ^{[1
]}

Surh, Young-Joon ^{[1
,2
,3
]}

机构：

[1] Seoul Natl Univ, Coll Pharm, Seoul 151742, South Korea

[2] Seoul Natl Univ, WCU Dept Mol Med & Biopharmaceut Sci, Grad Sch Convergence Sci & Technol, Seoul 151742, South Korea

[3] Seoul Natl Univ, Canc Res Inst, Seoul 151742, South Korea

来源：

MOLECULAR CARCINOGENESIS | 2011年 / 50卷 / 04期

基金：

新加坡国家研究基金会;

关键词：

p53; redox modulation; thiol modification; redox status; DNA-BINDING ACTIVITY; WILD-TYPE P53; SEQUENCE-SPECIFIC DNA; TUMOR-SUPPRESSOR P53; SENSITIVE TRANSCRIPTION FACTORS; INTERACTING PROTEIN KINASE-2; JUN NH2-TERMINAL KINASE; SMOOTH-MUSCLE CELLS; COLON-CANCER CELLS; OXIDATIVE STRESS;

D O I：

10.1002/mc.20709

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The tumor suppressor protein p53 functions as a stress-responsive transcription factor. In response to oxidative, nitrosative, and electrophilic insults, p53 undergoes post-translational modifications, such as oxidation and covalent modification of cysteines, nitration of tyrosines, acetylation of lysines, phosphorylation of serine/threonine residues, etc. Because p53 plays a vital role in the transcriptional regulation of genes encoding proteins involved in a wide spectrum of biochemical processes including DNA repair, cell-cycle regulation, and programmed cell death, the redox-modification of p53 appears to be an important determinant of cell fate. This review highlights the redox regulation of p53 and its consequences on cellular function. (C) 2011 Wiley-Liss, Inc.

引用

页码：222 / 234

页数：13

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