Huang Min, Miao Ze-Hong, Ding Jian
Divisn of Anti-tumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
Sheng Li Ke Xue Jin Zhan. 2007 Oct;38(4):295-300.
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.
DNA双链断裂（DSBs）是由许多外源性和内源性因素引起的主要细胞毒性损伤。为应对DSBs，细胞进化出了复杂且高度保守的系统，该系统主要由同源重组修复（HR）和非同源末端连接（NHEJ）途径组成，以有效修复这些致死性损伤。这两种途径在维持基因组完整性方面发挥着关键作用。在此，我们概述了这些途径中的详细过程、相关分子和调控因子。对DSBs修复的不断积累的认识可能为开发更有效的癌症治疗方法提供机会。
