K48 连接的泛素化和蛋白降解调控 53BP1 在 DNA 损伤部位的募集。
K48-linked ubiquitination and protein degradation regulate 53BP1 recruitment at DNA damage sites.
机构信息
Terry Fox Molecular Oncology Group and the Bloomfield Center for Research on Aging, Sir Mortimer B Davis Jewish General Hospital, Segal Cancer Centre, Lady Davis Institute for Medical Research, 3755 Côte Ste-Catherine Road, Montréal, Québec, H3T 1E2, Canada.
出版信息
Cell Res. 2012 Aug;22(8):1221-3. doi: 10.1038/cr.2012.58. Epub 2012 Apr 10.
Abstract
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.
摘要
高效的 DNA 损伤感知和修复对于维持基因组完整性至关重要，而无法检测或修复 DNA 断裂会导致突变，从而促进肿瘤的形成。介导 DNA 修复所必需的一种关键蛋白质是肿瘤抑制因子 53BP1。最近的研究表明，K48 连接的泛素化和蛋白质降解在 53BP1 募集到 DNA 损伤部位中起着至关重要的作用。
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