Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Radiat Res. 2014 Jan;181(1):1-8. doi: 10.1667/RR13572.1. Epub 2013 Dec 9.
The p53-binding protein 1 (53BP1) is a well-known DNA damage response (DDR) factor, which is recruited to nuclear structures at the site of DNA damage and forms readily visualized ionizing radiation (IR) induced foci. Depletion of 53BP1 results in cell cycle arrest in G2/M phase as well as genomic instability in human as well as mouse cells. Within the DNA damage response mechanism, 53BP1 is classified as an adaptor/mediator, required for processing of the DNA damage response signal and as a platform for recruitment of other repair factors. More recently, specific 53BP1 contributions to DSB repair pathway choice have been recognized and are being characterized. In this review, we have summarized recent advances in understanding the role of 53BP1 in regulating DNA DSBs repair pathway choice, variable diversity joining [V(D)J] recombination and class-switch recombination (CSR).
p53 结合蛋白 1（53BP1）是一种众所周知的 DNA 损伤反应（DDR）因子，它可被招募到 DNA 损伤部位的核结构中，并形成易于观察的电离辐射（IR）诱导焦点。53BP1 的耗竭会导致人类和小鼠细胞的 G2/M 期细胞周期停滞以及基因组不稳定性。在 DNA 损伤反应机制中，53BP1 被归类为一种衔接子/中介物，需要对 DNA 损伤反应信号进行处理，并作为招募其他修复因子的平台。最近，人们已经认识到 53BP1 对 DSB 修复途径选择的特定贡献，并正在对其进行表征。在这篇综述中，我们总结了对 53BP1 在调节 DNA DSBs 修复途径选择、可变多样性连接[V(D)J]重组和类别转换重组（CSR）中的作用的最新理解进展。
