DNA修复
DNA损伤
核苷酸切除修复
细胞生物学
DNA错配修复
Ku80型
雷达50
姐妹染色单体
复制后修复
DNA修复蛋白XRCC4
同源定向修复
化学
DNA
综合征如奈梅亨破损综合症
生物
DNA复制
遗传学
色素性干皮病
基因组不稳定性
细胞周期检查点
同源重组
非同源性末端接合
G2-M DNA损伤检查点
共济失调毛细血管扩张
细胞周期
DNA结合蛋白
细胞
染色体
基因
转录因子
出处
期刊:Journal of Zhejiang University-science B
[Springer Nature]
日期:2021-01-01
卷期号:22 (1): 31-37
被引量:19
标识
DOI:10.1631/jzus.b2000289
摘要
Genome stability can be threatened by both endogenous and exogenous agents. Organisms have evolved numerous mechanisms to repair DNA damage, including homologous recombination (HR) and non-homologous end joining (NHEJ). Among the factors associated with DNA repair, the MRE11-RAD50-NBS1 (MRN) complex (MRE11-RAD50-XRS2 in Saccharomyces cerevisiae) plays important roles not only in DNA damage recognition and signaling but also in subsequent HR or NHEJ repair. Upon detecting DNA damage, the MRN complex activates signaling molecules, such as the protein kinase ataxia-telangiectasia mutated (ATM), to trigger a broad DNA damage response, including cell cycle arrest. The nuclease activity of the MRN complex is responsible for DNA end resection, which guides DNA repair to HR in the presence of sister chromatids. The MRN complex is also involved in NHEJ, and has a species-specific role in hairpin repair. This review focuses on the structure of the MRN complex and its function in DNA damage repair.
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