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同源重组缺陷及其对复制叉维持的影响。

Homologous recombination defects and how they affect replication fork maintenance.

作者信息

Son Mi Young, Hasty Paul

机构信息

Department of Molecular Medicine and Institute of Biotechnology, UT Health San Antonio, 15355 Lambda Drive, San Antonio, USA.

The Mays Cancer Center, USA.

出版信息

AIMS Genet. 2019 Apr 3;5(4):192-211. doi: 10.3934/genet.2018.4.192. eCollection 2018.

Abstract

Homologous recombination (HR) repairs DNA double strand breaks (DSBs) and stabilizes replication forks (RFs). RAD51 is the recombinase for the HR pathway. To preserve genomic integrity, RAD51 forms a filament on the 3' end of a DSB and on a single-stranded DNA (ssDNA) gap. But unregulated HR results in undesirable chromosomal rearrangements. This review describes the multiple mechanisms that regulate HR with a focus on those mechanisms that promote and contain RAD51 filaments to limit chromosomal rearrangements. If any of these pathways break down and HR becomes unregulated then disease, primarily cancer, can result.

摘要

同源重组(HR)修复DNA双链断裂(DSB)并稳定复制叉(RF)。RAD51是HR途径的重组酶。为了维持基因组完整性,RAD51在DSB的3'末端和单链DNA(ssDNA)缺口上形成细丝。但是不受调控的HR会导致不良的染色体重排。本综述描述了调节HR的多种机制,重点关注那些促进和控制RAD51细丝以限制染色体重排的机制。如果这些途径中的任何一个发生故障并且HR变得不受调控,那么可能会导致疾病,主要是癌症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe85/6690234/089f5b1e96bd/genetics-05-04-192-g001.jpg

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