The impact of acetylation and deacetylation on the p53 pathway

被引:233
作者
Brooks, Christopher L. [1 ]
Gu, Wei [2 ,3 ]
机构
[1] Stemline Therapeut Inc, New York, NY 10128 USA
[2] Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA
[3] Columbia Univ, Coll Phys & Surg, Inst Canc Genet, New York, NY 10032 USA
关键词
p53; Mdm2; acetylation; deacetylation; destabilization; ubiquitination; transcriptional activation and stability; UBIQUITIN LIGASE ACTIVITY; DNA-BINDING DOMAIN; IN-VIVO; POSTTRANSLATIONAL MODIFICATIONS; REGULATES APOPTOSIS; EMBRYONIC LETHALITY; MDM2-DEFICIENT MICE; NEGATIVE REGULATOR; TUMOR-SUPPRESSOR; ACTIVATES P53;
D O I
10.1007/s13238-011-1063-9
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
The p53 tumor suppressor is a sequence-specific transcription factor that undergoes an abundance of post-translational modifications for its regulation and activation. Acetylation of p53 is an important reversible enzymatic process that occurs in response to DNA damage and genotoxic stress and is indispensible for p53 transcriptional activity. p53 was the first non-histone protein shown to be acetylated by histone acetyl transferases, and a number of more recent in vivo models have underscored the importance of this type of modification for p53 activity. Here, we review the current knowledge and recent findings of p53 acetylation and deacetylation and discuss the implications of these processes for the p53 pathway.
引用
收藏
页码:456 / 462
页数:7
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