PMID- 28847818
OWN - NLM
STAT- MEDLINE
DCOM- 20180404
LR  - 20240210
IS  - 1471-2970 (Electronic)
IS  - 0962-8436 (Print)
IS  - 0962-8436 (Linking)
VI  - 372
IP  - 1731
DP  - 2017 Oct 5
TI  - SUMO, a small, but powerful, regulator of double-strand break repair.
LID - 10.1098/rstb.2016.0281 [doi]
LID - 20160281
AB  - The response to a DNA double-stranded break in mammalian cells is a process of 
      sensing and signalling the lesion. It results in halting the cell cycle and local 
      transcription and in the mediation of the DNA repair process itself. The response 
      is launched through a series of post-translational modification signalling events 
      coordinated by phosphorylation and ubiquitination. More recently modifications of 
      proteins by Small Ubiquitin-like MOdifier (SUMO) isoforms have also been found to 
      be key to coordination of the response (Morris et al. 2009 Nature462, 886-890 
      (doi:10.1038/nature08593); Galanty et al. 2009 Nature462, 935-939 
      (doi:10.1038/nature08657)). However our understanding of the role of SUMOylation 
      is slight compared with our growing knowledge of how ubiquitin drives signal 
      amplification and key chromatin interactions. In this review we consider our 
      current knowledge of how SUMO isoforms, SUMO conjugation machinery, SUMO 
      proteases and SUMO-interacting proteins contribute to directing altered chromatin 
      states and to repair-protein kinetics at a double-stranded DNA lesion in 
      mammalian cells. We also consider the gaps in our understanding.This article is 
      part of the themed issue 'Chromatin modifiers and remodellers in DNA repair and 
      signalling'.
CI  - (c) 2017 The Author(s).
FAU - Garvin, Alexander J
AU  - Garvin AJ
AD  - Birmingham Centre for Genome Biology and Institute of Cancer and Genomic 
      Sciences, Medical and Dental School, University of Birmingham, Edgbaston, 
      Birmingham B15 2TT, UK.
FAU - Morris, Joanna R
AU  - Morris JR
AUID- ORCID: 0000-0001-9762-8133
AD  - Birmingham Centre for Genome Biology and Institute of Cancer and Genomic 
      Sciences, Medical and Dental School, University of Birmingham, Edgbaston, 
      Birmingham B15 2TT, UK j.morris.3@bham.ac.uk.
LA  - eng
GR  - 19062/CRUK_/Cancer Research UK/United Kingdom
PT  - Journal Article
PT  - Review
PL  - England
TA  - Philos Trans R Soc Lond B Biol Sci
JT  - Philosophical transactions of the Royal Society of London. Series B, Biological 
      sciences
JID - 7503623
RN  - 0 (Small Ubiquitin-Related Modifier Proteins)
SB  - IM
MH  - Animals
MH  - *DNA Breaks, Double-Stranded
MH  - *DNA Repair
MH  - Humans
MH  - Mammals/*genetics
MH  - Small Ubiquitin-Related Modifier Proteins/*metabolism
MH  - *Sumoylation
PMC - PMC5577459
OTO - NOTNLM
OT  - SUMO
OT  - SUMO protease
OT  - double-strand break repair
OT  - ubiquitin
COIS- The authors have no competing interests.
EDAT- 2017/08/30 06:00
MHDA- 2018/04/05 06:00
PMCR- 2017/08/28
CRDT- 2017/08/30 06:00
PHST- 2017/04/05 00:00 [accepted]
PHST- 2017/08/30 06:00 [entrez]
PHST- 2017/08/30 06:00 [pubmed]
PHST- 2018/04/05 06:00 [medline]
PHST- 2017/08/28 00:00 [pmc-release]
AID - rstb.2016.0281 [pii]
AID - rstb20160281 [pii]
AID - 10.1098/rstb.2016.0281 [doi]
PST - ppublish
SO  - Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731):20160281. doi: 
      10.1098/rstb.2016.0281.