摘要
多种内源或外源因素都能造成细胞基因组DNA损伤,细胞内建立了复杂的修复系统来应对不同形式的损伤。其中DNA双链断裂(DNA double-strand breaks,DSBs)作为最严重的损伤形式,主要激活同源重组修复(Homologous recombination repair)和非同源末端连接(Non-homologous end joining)通路。这两条通路都是由多个修复元件参与、经过多步反应的复杂过程。两者各具特点、协同作用,共同维护细胞基因组的稳定性。对其分子机制的阐明为肿瘤放化疗的辅助治疗提供了潜在的作用靶点。
DNA double-strand breaks （ DSBs ） are the principal cytotoxic lesions caused by many exogenous and endogenous factors. In response to DSBs, cells have evolved complex and highly conserved systems, which mainly consist of homologous recombination repair （ HR ） and non-homologous end joining （ NHEJ ） pathways, to effectively repair the lethal lesions. The two pathways play crucial roles in preserving the genomic integrity. Here, we provide an overview of detailed process, concerned molecules and regulatory factors in these pathways. Accumulated knowledge of DSBs repair may offer opportunities to develop more effective treatments for cancer.
出处
《生理科学进展》
CAS
CSCD
北大核心
2007年第4期295-300,共6页
Progress in Physiological Sciences
基金
中国科学院知识创新工程项目资助课题(KSX1-SW-11-6)
关键词
DNA双链断裂
修复通路
同源重组修复
非同源末端连接
DNA double-strand breaks
repair pathways
homologous recombination repair
non-homologous end joining
