Downloads: 314

Files in This Item:
File Description SizeFormat 
ggs.15-00010.pdf342.86 kBAdobe PDFView/Open
Title: Chromatin modification and NBS1: Their relationship in DNA double-strand break repair
Authors: Saito, Yuichiro
Zhou, Hui
Kobayashi, Junya  KAKEN_id
Author's alias: 小林, 純也
Keywords: Chromatin
DNA double-strand break
DNA repair
Histone modification
NBS1
Issue Date: 2015
Publisher: Genetics Society of Japan
Journal title: Genes & Genetic Systems
Volume: 90
Issue: 4
Start page: 195
End page: 208
Abstract: The importance of chromatin modification, including histone modification and chromatin remodeling, for DNA double-strand break (DSB) repair, as well as transcription and replication, has been elucidated. Phosphorylation of H2AX to γ-H2AX is one of the first responses following DSB detection, and this histone modification is important for the DSB damage response by triggering several events, including the accumulation of DNA damage response-related proteins and subsequent homologous recombination (HR) repair. The roles of other histone modifications such as acetylation, methylation and ubiquitination have also been recently clarified, particularly in the context of HR repair. NBS1 is a multifunctional protein that is involved in various DNA damage responses. Its recently identified binding partner RNF20 is an E3 ubiquitin ligase that facilitates the monoubiquitination of histone H2B, a process that is crucial for recruitment of the chromatin remodeler SNF2h to DSB damage sites. Evidence suggests that SNF2h functions in HR repair, probably through regulation of end-resection. Moreover, several recent reports have indicated that SNF2h can function in HR repair pathways as a histone remodeler and that other known histone remodelers can also participate in DSB damage responses. On the other hand, information about the roles of such chromatin modifications and NBS1 in non-homologous end joining (NHEJ) repair of DSBs and stalled fork-related damage responses is very limited; therefore, these aspects and processes need to be further studied to advance our understanding of the mechanisms and molecular players involved.
Rights: © 2015, Genetics Society of Japan. All rights reserved.
Publisher permitted posting the file of publiser's version on this repositry.
発行元の許可を得て登録しています.
URI: http://hdl.handle.net/2433/224789
DOI(Published Version): 10.1266/ggs.15-00010
PubMed ID: 26616756
Appears in Collections:Journal Articles

Show full item record

Export to RefWorks


Export Format: 


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.