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

被引:0
|
作者
Frédérick A Mallette
Stéphane Richard
机构
[1] Terry Fox Molecular Oncology Group and the Bloomfield Center for Research on Aging,Departments of Medicine and Oncology
[2] Sir Mortimer B Davis Jewish General Hospital,undefined
[3] Segal Cancer Centre,undefined
[4] Lady Davis Institute for Medical Research,undefined
[5] McGill University,undefined
来源
Cell Research | 2012年 / 22卷
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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.
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页码:1221 / 1223
页数:2
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