2015 Fiscal Year Final Research Report
Analysis of mechanisms to tolerate for DNA replication blockage at DNA lesions
Project/Area Number |
25241011
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Research Category |
Grant-in-Aid for Scientific Research (A)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Risk sciences of radiation and chemicals
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Research Institution | Nagoya University |
Principal Investigator |
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Co-Investigator(Renkei-kenkyūsha) |
Masuda Yuji 名古屋大学, 環境医学研究所, 准教授 (30273866)
Kanao Rie 名古屋大学, 環境医学研究所, 助教 (30542287)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | DNA損傷 / 損傷乗り越え複製 / Polh / PCNA / 翻訳後修飾 |
Outline of Final Research Achievements |
In human cells, multiple units of a PCNA homo-trimer are simultaneously mono-ubiquitinated at K164, which could activate unidentified mechanisms other than Polh-mediated translesion synthesis to replicate damaged DNA. Human Polh contains three PCNA-interacting motifs and a ubiquitin-interacting domain, all of which are included in the regulation of Polh-mediated translesion synthesis in a cooperative and redundant manner. A deubiquitinating enzyme, USP1, plays a crucial role in the regulation of DNA replication-coupled translesion DNA synthesis past UV-induced DNA lesions. USP7 is also involved in the PCNA deubiquitination and suppresses oxidative-stress-induced mutagenesis.
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Free Research Field |
分子生物学
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