DNA-Protein Crosslinks and Their Resolution

被引：39

作者：

Weickert, Pedro ^{[1
,2
]}

Stingele, Julian ^{[1
,2
]}

机构：

[1] Ludwig Maximilians Univ Munchen, Dept Biochem, Munich, Germany

[2] Ludwig Maximilians Univ Munchen, Gene Ctr, Munich, Germany

来源：

ANNUAL REVIEW OF BIOCHEMISTRY | 2022年 / 91卷

基金：

欧洲研究理事会;

关键词：

UBIQUITIN LIGASE RFWD3; DOUBLE-STRAND BREAKS; TOPOISOMERASE-II; SPINOCEREBELLAR ATAXIA; RAD32(MRE11) NUCLEASE; HISTONE DEMETHYLATION; COVALENT COMPLEXES; DAMAGE RESPONSE; EXCISION-REPAIR; DVC1; C1ORF124;

D O I：

10.1146/annurev-biochem-032620-105820

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：

Covalent DNA-protein crosslinks (DPCs) are pervasive DNA lesions that interfere with essential chromatin processes such as transcription or replication. This review strives to provide an overview of the sources and principles of cellular DPC formation. DPCs are caused by endogenous reactive metabolites and various chemotherapeutic agents. However, in certain conditions DPCs also arise physiologically in cells. We discuss the cellular mechanisms resolving these threats to genomic integrity. Detection and repair of DPCs require not only the action of canonical DNA repair pathways but also the activity of specialized proteolytic enzymes-including proteases of the SPRTN/Wss1 family-to degrade the crosslinked protein. Loss of DPC repair capacity has dramatic consequences, ranging from genome instability in yeast and worms to cancer predisposition and premature aging in mice and humans.

引用

页码：157 / 181

页数：25

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