Canonical DNA Repair Pathways Influence R-Loop-Driven Genome Instability

被引：32

作者：

Stirling, Peter C. ^{[1
,2
]}

Hieter, Philip ^{[2
,3
]}

机构：

[1] BC Canc Agcy, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada

[2] Univ British Columbia, Dept Med Genet, Vancouver, BC V6H 3N1, Canada

[3] Univ British Columbia, Michael Smith Labs, Vancouver, BC V6T 1Z4, Canada

来源：

JOURNAL OF MOLECULAR BIOLOGY | 2017年 / 429卷 / 21期

基金：

加拿大健康研究院;

关键词：

Genome Instability; R-loops; DNA repair; Fanconi Anemia; Fork protection; TRANSCRIPTION-REPLICATION CONFLICTS; FANCONI-ANEMIA; EXCISION-REPAIR; HOMOLOGOUS RECOMBINATION; STABILITY; INACTIVATION; CHROMATIN; COOPERATE; INTEGRITY; PRODUCTS;

D O I：

10.1016/j.jmb.2016.07.014

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

DNA repair defects create cancer predisposition in humans by fostering a higher rate of mutations. While DNA repair is quite well characterized, recent studies have identified previously unrecognized relationships between DNA repair and R-loop-mediated genome instability. R-loops are three-stranded nucleic acid structures in which RNA binds to genomic DNA to displace a loop of single-stranded DNA. Mutations in homologous recombination, nucleotide excision repair, crosslink repair, and DNA damage checkpoints have all now been linked to formation and function of transcription-coupled R-loops. This perspective will summarize recent literature linking DNA repair to R-loop-mediated genomic instability and discuss how R-loops may contribute to mutagenesis in DNA-repair-deficient cancers. (C) 2016 Elsevier Ltd. All rights reserved.

引用

页码：3132 / 3138

页数：7

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