Ubiquitin and SUMO signalling in DNA repair

被引：25

作者：

Thomson, Timothy M. ^{[1
]}

Guerra-Rebollo, Marta ^{[1
]}

机构：

[1] CSIC, Inst Biol Mol Barcelona, Dept Cell Biol, Lab Cell Signaling & Canc, E-08028 Barcelona, Spain

来源：

BIOCHEMICAL SOCIETY TRANSACTIONS | 2010年 / 38卷

关键词：

DNA damage; DNA repair; phosphorylation; small ubiquitin-related modifier (SUMO); ubiquitin; NUCLEOTIDE EXCISION-REPAIR; REPLICATION PROTEIN-A; SENSOR RAD9-RAD1-HUS1 INTERACTS; CANCER-PREDISPOSING MUTATIONS; HOMOLOGY-DIRECTED REPAIR; DOUBLE-STRAND BREAKS; UV-DAMAGED DNA; FANCONI-ANEMIA; LIGASE ACTIVITY; POLYUBIQUITIN CHAINS;

D O I：

10.1042/BST0380116

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：

The repair of lesions and gaps in DNA follows different pathways, each mediated by specific proteins and complexes. Post-translational modifications in many of these proteins govern their activities and interactions, ultimately determining whether a particular pathway is followed. Prominent among these modifications are the addition of phosphate or ubiquitin (and ubiquitin-like) moieties that confer new binding surfaces and conformational states on the modified proteins. The present review summarizes some of consequences of ubiquitin and ubiquitin-like modifications and interactions that regulate nucleotide excision repair, translesion synthesis, double-strand break repair and interstrand cross-link repair, with the discussion of relevant examples in each pathway.

引用

页码：116 / 131

页数：16

共 186 条

[51] The UBA2 domain functions as an intrinsic stabilization signal that protects Rad23 from proteasomal degradation [J].