Departments of Biochemistry and Molecular Biology and Oncology, and Southern Alberta Cancer Research Institute, University of Calgary, Calgary, Canada.
Int J Radiat Oncol Biol Phys. 2013 Jul 1;86(3):440-9. doi: 10.1016/j.ijrobp.2013.01.011. Epub 2013 Feb 20.
DNA damage can occur as a result of endogenous metabolic reactions and replication stress or from exogenous sources such as radiation therapy and chemotherapy. DNA double strand breaks are the most cytotoxic form of DNA damage, and defects in their repair can result in genome instability, a hallmark of cancer. The major pathway for the repair of ionizing radiation-induced DSBs in human cells is nonhomologous end joining. Here we review recent advances on the mechanism of nonhomologous end joining, as well as new findings on its component proteins and regulation.
DNA 损伤可能是由于内源性代谢反应和复制应激引起的，也可能是由于外源性因素如放射治疗和化疗引起的。DNA 双链断裂是最具细胞毒性的 DNA 损伤形式，其修复缺陷可导致基因组不稳定，这是癌症的一个标志。在人类细胞中修复电离辐射诱导的 DSB 的主要途径是非同源末端连接。本文综述了非同源末端连接机制的最新进展，以及其组成蛋白和调控的新发现。
