《生命科学》 2014, 26(11): 1172-1175
摘 要：摘 要：在各种DNA 损伤中，DNA 双链断裂(double-strand break， DSB) 是最为严重的一种，快速准确地修复DSB 对维持基因组稳定性起着至关重要的作用。真核生物细胞通过一系列复杂的信号转导途径激活对DSB 的修复，其中最为重要的是同源重组和非同源末端连接机制。最近的研究表明，这两种方式在DSB修复的早期是相互竞争的关系，其选择在很大程度上受到53BP1 及同源蛋白质的调控。将讨论53BP1 作为DSB 修复途径的核心因子，在染色质水平整合BRCA1、CtIP 等修复因子和多种组蛋白修饰构成的信号途径，介导同源重组和非同源末端连接通路选择的分子机制。
Abstract: Abstract: Double-strand break (DSB) is the most serious one in all kinds of DNA damage. Rapid repair of DSB is essential for genome stability. In eukaryotic cells，DSB repair is activated via a series of signal transduction，and homologous recombination and non-homologous end joining are most important. Recent research shows that the two pathways are competitive at the early period of DSB repair， the choice between them is largely regulated by 53BP1 and its homologous proteins. This review will discuss the novel mechanism that 53BP1， as a key factor in DSB repair， integrates the signal pathway including BRCA1/CtIP and multiple histone modifications， thereby regulating the choice between homologous recombination and non-homologous end joining.
