同源重组缺陷及其对复制叉维持的影响

AIMS Genetics Pub Date : 2019-04-03 eCollection Date: 2018-01-01 DOI:10.3934/genet.2018.4.192
Mi Young Son, Paul Hasty
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引用次数: 0

摘要

摘要同源重组(HR)修复DNA双链断裂(DSBs)并稳定复制叉(RFs)。RAD51是HR途径的重组酶。为了保持基因组的完整性,RAD51在DSB的3〃末端和单链DNA(ssDNA)间隙上形成细丝。但不受调控的HR会导致不理想的染色体重排。这篇综述描述了调节HR的多种机制,重点是那些促进并含有RAD51丝以限制染色体重排的机制。如果这些途径中的任何一种被破坏,HR变得不受控制,那么可能会导致疾病,主要是癌症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Homologous recombination defects and how they affect replication fork maintenance.

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.

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AIMS Genetics
AIMS Genetics GENETICS & HEREDITY-
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