Roles of newly discovered NBS1 domains in ubiquitin signals and rejoining of double-strand breaks after irradiation

2014 Fiscal Year Final Research Report

• Project/Area Number: 23241021
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Risk sciences of radiation/Chemicals
• Research Institution: Kyoto University
• Principal Investigator: KOMATSU Kenshi 京都大学, 放射線生物研究センター, 教授 (80124577)
• Co-Investigator(Kenkyū-buntansha): KOBAYASHI Junya 京都大学, 放射線生物研究センター, 准教授 (30301302) ; KATO Akihiro 京都大学, 放射線生物研究センター, 研究員 (70423051)
• Project Period (FY): 2011-04-01 – 2015-03-31
• Keywords: 損傷乗越えDNA合成 / NBS1

Outline of Final Research Achievements

NBS1, a protein responsible for radiation sensitive disorder, has been to control both cell cycle checkpoint and homologous recombination repair by binding to either ATM or MRE11 at the C-terminus of NBS1. We hosed here other two binding regions at the C-terminus and their regulatory mechanisms. NBS1 ubiquitinates PCNA and then initiates Pol eta-mediated translesional DNA synthesis by binding to RAD18. It also binding to RNF20 to ubiquitinate histone H2B, which,in turn, recruits histone chaperon FACT and initiates chromatin-remodeling for rejoining of DNA double-strand break.

Free Research Field

放射線生物学