DNA double-strand break repair： a tale of pathway choices  

作　　者：Jing Li Xingzhi Xu 

机构地区：[1]Beijing Key Laboratory of DNA Damage Response and College of Life Sciences, Capital Normal University, Beijing100048, China

出　　处：《Acta Biochimica et Biophysica Sinica》2016年第7期641-646,共6页生物化学与生物物理学报（英文版）

基　　金：This work was supported by the grants from the National Natural Science Foundation of China （Nos. 31461143012 and 31530016）, the National Basic Research Program of China （Nos. 2013CB911002 and 2015CB910601） to X.X., and from Young Talent Development Plan in Institutions of Higher Learning under the Jurisdiction of Beijing Municipality （No. CIT＆TCD201404158） and Beijing Nova Program Interdisciplinary Cooperation Project to J.L.

摘　　要：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.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.

关 键 词：DSB 53BP1 RIF1 PTIP BRCA1 

分 类 号：Q523[生物学—生物化学] TQ172.632[化学工程—水泥工业]