Li Jing, Xu Xingzhi
Beijing Key Laboratory of DNA Damage Response and College of Life Sciences, Capital Normal University, Beijing 100048, China
Acta Biochim Biophys Sin (Shanghai). 2016 Jul;48(7):641-6. doi: 10.1093/abbs/gmw045. Epub 2016 May 23.
Deoxyribonucleic acid double-strand breaks (DSBs) are cytotoxic lesions that must be repaired either through homologous recombination (HR) or non-homologous end-joining (NHEJ) pathways. DSB repair is critical for genome integrity, cellular homeostasis and also constitutes the biological foundation for radiotherapy and the majority of chemotherapy. The choice between HR and NHEJ is a complex yet not completely understood process that will entail more future efforts. Herein we review our current understandings about how the choice is made over an antagonizing balance between p53-binding protein 1 and breast cancer 1 in the context of cell cycle stages, downstream effects, and distinct chromosomal histone marks. These exciting areas of research will surely bring more mechanistic insights about DSB repair and be utilized in the clinical settings.
脱氧核糖核酸双链断裂（DSB）是具有细胞毒性的损伤，必须通过同源重组（HR）或非同源末端连接（NHEJ）途径进行修复。DSB修复对于基因组完整性、细胞稳态至关重要，也是放射治疗和大多数化疗的生物学基础。HR和NHEJ之间的选择是一个复杂但尚未完全理解的过程，未来还需要更多的努力。在此，我们综述了目前对于在细胞周期阶段、下游效应以及不同染色体组蛋白标记的背景下，p53结合蛋白1和乳腺癌1之间如何通过拮抗平衡做出选择的理解。这些令人兴奋的研究领域肯定会带来更多关于DSB修复的机制性见解，并应用于临床实践。
