Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis

被引：719

作者：

Moynahan, Mary Ellen ^{[1
,2
]}

Jasin, Maria ^{[1
]}

机构：

[1] Mem Sloan Kettering Canc Ctr, Dev Biol Program, New York, NY 10065 USA

[2] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10065 USA

来源：

NATURE REVIEWS MOLECULAR CELL BIOLOGY | 2010年 / 11卷 / 03期

关键词：

DOUBLE-STRAND BREAKS; DNA-END RESECTION; HUMAN RAD51 PROTEIN; FANCONI-ANEMIA; DIRECTED REPAIR; BIALLELIC MUTATIONS; GENE CONVERSION; BRCT DOMAIN; EMBRYONIC LETHALITY; STRUCTURAL BASIS;

D O I：

10.1038/nrm2851

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Mitotic homologous recombination promotes genome stability through the precise repair of DNA double-strand breaks and other lesions that are encountered during normal cellular metabolism and from exogenous insults. As a result, homologous recombination repair is essential during proliferative stages in development and during somatic cell renewal in adults to protect against cell death and mutagenic outcomes from DNA damage. Mutations in mammalian genes encoding homologous recombination proteins, including BRCA1, BRCA2 and PALB2, are associated with developmental abnormalities and tumorigenesis. Recent advances have provided a clearer understanding of the connections between these proteins and of the key steps of homologous recombination and DNA strand exchange.

引用

页码：196 / 207

页数：12

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