K48-linked ubiquitination and protein degradation regulate 53BP1 recruitment at DNA damage sites

被引：52

作者：

Mallette, Frederick A. ^{[1
,2
,3
,4
]}

Richard, Stephane ^{[1
,2
,3
,4
]}

机构：

[1] Sir Mortimer B Davis Jewish Hosp, Lady Davis Inst Med Res, Segal Canc Ctr, Terry Fox Mol Oncol Grp, Montreal, PQ H3T 1E2, Canada

[2] Sir Mortimer B Davis Jewish Hosp, Lady Davis Inst Med Res, Segal Canc Ctr, Bloomfield Ctr Res Aging, Montreal, PQ H3T 1E2, Canada

[3] McGill Univ, Dept Med, Montreal, PQ, Canada

[4] McGill Univ, Dept Oncol, Montreal, PQ, Canada

来源：

CELL RESEARCH | 2012年 / 22卷 / 08期

基金：

加拿大健康研究院;

关键词：

REPAIR; ACCUMULATION; METHYLATION; RECOGNITION; L3MBTL1;

D O I：

10.1038/cr.2012.58

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Efficient DNA damage sensing and repair is crucial to preserve genomic integrity and failure to detect or repair DNA breaks can cause mutations, contributing to the formation of tumors. One key protein required for mediating DNA repair is the tumor suppressor 53BP1. Recent studies now demonstrate the crucial role of K48-linked ubiquitination and protein degradation for 53BP1 recruitment at sites of DNA damage.

引用

页码：1221 / 1223

页数：3

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