雷达51
同源重组
生物
突变体
DNA修复
分子生物学
野生型
细胞生物学
基因
遗传学
作者
Carmen Arias‐Lopez,Iciar Lazaro‐Trueba,Peter Kerr,Christopher J. Lord,Tim Dexter,Marjan Iravani,Alan Ashworth,Augusto Silva
出处
期刊:EMBO Reports
[Springer Nature]
日期:2005-12-02
卷期号:7 (2): 219-224
被引量:193
标识
DOI:10.1038/sj.embor.7400587
摘要
DNA repair by homologous recombination is involved in maintaining genome stability. Previous data report that wild‐type p53 suppresses homologous recombination and physically interacts with Rad51. Here, we show the in vivo binding of wild‐type p53 to a p53 response element in the promoter of Rad51 and the downregulation of Rad51 messenger RNA and protein by wild‐type p53, favoured by DNA damage. Moreover, wild‐type p53 inhibits Rad51 foci formation in response to double‐strand breaks, whereas p53 contact mutant R280K fails to repress Rad51 mRNA and protein expression and Rad51 foci formation. We propose that transcriptional repression of Rad51 by p53 participates in regulating homologous recombination, and impaired Rad51 repression by p53 mutants may contribute to malignant transformation.
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