College of Veterinary Medicine, Department of Microbiology & Molecular Genetics, Michigan State University, East Lansing, Michigan 48824, United States.
Mutat Res. 2011 Jun 3;711(1-2):73-86. doi: 10.1016/j.mrfmmm.2011.02.010. Epub 2011 Mar 3.
DNA double-strand breaks are extremely harmful lesions that can lead to genomic instability and cell death if not properly repaired. There are at least three pathways that are responsible for repairing DNA double-strand breaks in mammalian cells: non-homologous end joining, homologous recombination and alternative non-homologous end joining. Here we review each of these three pathways with an emphasis on the role of the DNA-dependent protein kinase, a critical component of the non-homologous end joining pathway, in influencing which pathway is ultimately utilized for repair.
DNA 双链断裂是极其有害的损伤，如果不能得到妥善修复，可能导致基因组不稳定和细胞死亡。哺乳动物细胞中至少有三种途径负责修复 DNA 双链断裂：非同源末端连接、同源重组和替代性非同源末端连接。本文重点介绍了非同源末端连接途径中的关键组成部分——依赖于 DNA 的蛋白激酶，综述了这三种途径，并讨论了其对最终修复途径选择的影响。
