Blinded by the Light: The Growing Complexity of p53

被引:2456
作者
Vousden, Karen H. [1 ]
Prives, Carol [2 ]
机构
[1] Beatson Inst Canc Res, Glasgow G61 1BD, Lanark, Scotland
[2] Columbia Univ, Dept Biol Sci, New York, NY 10027 USA
关键词
TUMOR-SUPPRESSOR P53; CELL-CYCLE ARREST; INTERACTING PROTEIN KINASE-2; CAENORHABDITIS-ELEGANS P53; FACTOR-BINDING-SITES; DNA-DAMAGE; IN-VIVO; GENE-EXPRESSION; P53-MEDIATED APOPTOSIS; POSTTRANSLATIONAL MODIFICATIONS;
D O I
10.1016/j.cell.2009.04.037
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
While the tumor suppressor functions of p53 have long been recognized, the contribution of p53 to numerous other aspects of disease and normal life is only now being appreciated. This burgeoning range of responses to p53 is reflected by an increasing variety of mechanisms through which p53 can function, although the ability to activate transcription remains key to p53's modus operandi. Control of p53's transcriptional activity is crucial for determining which p53 response is activated, a decision we must understand if we are to exploit efficiently the next generation of drugs that selectively activate or inhibit p53.
引用
收藏
页码:413 / 431
页数:19
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