K48-1inked ubiquitination and protein degradation regulate 53BP1 recruitment at DNA damage sites  

作　　者：Frederick A Mallette 

机构地区：[1]Terry Fox Molecular Oncology Group and the Bloomfield Center for Research on Aging, Sir Mortimer B Davis Jewish GeneralHospital, Segal Cancer Centre, Lady Davis Institute for Medical Research, 3 755 C6te Ste-Catherine Road, Montreal, QuObec, H3T1E2, Canada, [2]Departments of Medicine and Oncology, McGill University, Montrdal, QuObec, Canada

出　　处：《Cell Research》2012年第8期1221-1223,共3页细胞研究（英文版）

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 K48-1inked ubiqnitination and pro- tein degradation for 53BPI recruitment at sites of DNA damage.

关 键 词：DNA损伤 蛋白降解 泛素化 DNA修复 肿瘤抑制 DNA断裂 蛋白质降解 基因突变 

分 类 号：Q523[生物学—生物化学] Q26