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
收藏
页码：3132 / 3138
页数：7
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