The MRE11 complex: starting from the ends

被引:536
作者
Stracker, Travis H. [1 ]
Petrini, John H. J. [2 ]
机构
[1] Inst Res Biomed IRB Barcelona, Barcelona 08028, Spain
[2] Mem Sloan Kettering Canc Ctr, New York, NY 10065 USA
基金
美国国家卫生研究院;
关键词
STRAND-BREAK REPAIR; DNA-DAMAGE RESPONSE; S-PHASE CHECKPOINT; TELANGIECTASIA-LIKE DISORDER; CLASS-SWITCH RECOMBINATION; DEPENDENT PROTEIN-KINASE; SACCHAROMYCES-CEREVISIAE; ATAXIA-TELANGIECTASIA; FANCONI-ANEMIA; MRN COMPLEX;
D O I
10.1038/nrm3047
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The maintenance of genome stability depends on the DNA damage response (DDR), which is a functional network comprising signal transduction, cell cycle regulation and DNA repair. The metabolism of DNA double-strand breaks governed by the DDR is important for preventing genomic alterations and sporadic cancers, and hereditary defects in this response cause debilitating human pathologies, including developmental defects and cancer. The MRE11 complex, composed of the meiotic recombination 11 (MRE11), RAD50 and Nijmegen breakage syndrome 1 (NBS1; also known as nibrin) proteins is central to the DDR, and recent insights into its structure and function have been gained from in vitro structural analysis and studies of animal models in which the DDR response is deficient.
引用
收藏
页码:90 / 103
页数:14
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