Litvinov S V
Tsitol Genet. 2014 May-Jun;48(3):64-77.
Double-strand DNA breaks (DSBs) resulting from cellular metabolic processes and external factors are a serious threat to the stability of the genome. Therefore, the cells have different molecular mechanisms for the efficient repair of this type of dá-mage. In this review we consider two main biochemical pathways of double-strand DNA breaks repair in eukaryotic cells--DNA strands nonhomologous end joining and homologous recombination between sister chromatids or chromatids of homologous chromosomes. Numerous data obtained recently for various eukaryotic cells suggest that complex interplay between the major DSB repair pathways normally facilitate the efficient repair and maintenance of the structural and functional genome integrity, but at the same time, under conditions ofgenotoxic factors exposure may induce increased genomic instability.
由细胞代谢过程和外部因素导致的双链DNA断裂（DSB）对基因组的稳定性构成严重威胁。因此，细胞具有不同的分子机制来有效修复这类损伤。在本综述中，我们探讨真核细胞中双链DNA断裂修复的两种主要生化途径——DNA链的非同源末端连接以及姐妹染色单体或同源染色体染色单体之间的同源重组。最近从各种真核细胞获得的大量数据表明，主要DSB修复途径之间的复杂相互作用通常有助于高效修复并维持基因组结构和功能的完整性，但同时，在暴露于基因毒性因素的条件下可能会导致基因组不稳定性增加。
