DNA double-strand breaks as drivers of neural genomic change, function, and disease

被引：71
作者：
Alt, Frederick W. [1 ,2 ]
Schwer, Bjoern [3 ,4 ]
机构：
[1] Harvard Med Sch, Howard Hughes Med Inst, Program Cellular & Mol Med, Dept Genet,Boston Childrens Hosp, Boston, MA 02115 USA
[2] Harvard Med Sch, Dept Pediat, Boston, MA 02115 USA
[3] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA 94158 USA
[4] Univ Calif San Francisco, Eli & Edythe Broad Ctr Regenerat Med & Stem Cell, San Francisco, CA 94158 USA
来源：
DNA REPAIR | 2018年 / 71卷
关键词：
DNA repair; Non-homologous end joining; DNA double-strand breaks; Neural stem and progenitor cells; Neurons; Somatic mosaicism; Exon shuffling; Genomic instability; DNA replication; Transcription; Neurodevelopment; Copy number variations; END-JOINING PROTEINS; COMMON FRAGILE SITES; V(D)J RECOMBINATION; NERVOUS-SYSTEM; CHROMOSOMAL TRANSLOCATIONS; STEM/PROGENITOR CELLS; EMBRYONIC LETHALITY; SEQUENCING REVEALS; LIGASE IV; B-CELLS;
D O I：
10.1016/j.dnarep.2018.08.019
中图分类号：
Q3 [遗传学];
学科分类号：
071007 ; 090102 ;
摘要：
Early work from about two decades ago implicated DNA double-strand break (DSB) formation and repair in neuronal development. Findings emerging from recent studies of DSBs in proliferating neural progenitors and in mature, non-dividing neurons suggest important roles of DSBs in brain physiology, aging, cancer, psychiatric and neurodegenerative disorders. We provide an overview of some findings and speculate on what may lie ahead.
引用
收藏
页码：158 / 163
页数：6
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