p53 post-translational modification: deregulated in tumorigenesis

被引:417
作者
Dai, Chao [1 ,2 ]
Gu, Wei [1 ,3 ]
机构
[1] Columbia Univ Coll Phys & Surg, Inst Canc Genet, New York, NY 10032 USA
[2] Columbia Univ, Dept Biol Sci, New York, NY 10027 USA
[3] Columbia Univ Coll Phys & Surg, Dept Pathol & Cell Biol, New York, NY 10032 USA
关键词
IN-VIVO; CELL-CYCLE; P53-DEPENDENT APOPTOSIS; SER46; PHOSPHORYLATION; NEGATIVE REGULATOR; EXPRESSION; ACETYLATION; PROTEIN; GENE; LIGASE;
D O I
10.1016/j.molmed.2010.09.002
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 p53 tumor suppressor protein has well-established roles in monitoring various types of stress signals by activating specific transcriptional targets that control cell cycle arrest and apoptosis, although some activities are also mediated in a transcription-independent manner. Here, we review the recent advances in our understanding of the wide spectrum of post-translational modifications that act as epigenetic-like codes for modulating specific functions of p53 in vivo and how deregulation of these modifications might contribute to tumorigenesis. We also discuss future research priorities to further understand p53 post-translational modifications and the interpretation of genetic data in appreciation of the increasing evidence that p53 regulates cellular metabolism, autophagy and many unconventional tumor suppressor activities.
引用
收藏
页码:528 / 536
页数:9
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