2016 Fiscal Year Final Research Report
Rescue of arrested replication forks by multiple ubiquitination of PCNA
Project/Area Number |
26740017
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Risk sciences of radiation and chemicals
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Research Institution | Nagoya University |
Principal Investigator |
Kanao Rie 名古屋大学, 環境医学研究所, 助教 (30542287)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | DNA損傷トレランス / PCNA / モノユビキチン化 / 損傷乗り越え複製 |
Outline of Final Research Achievements |
DNA damage tolerance is an important mechanism to prevent DNA replication arrest by DNA damage. It is suggested that DNA damage tolerance is regulated by post-translational modifications of PCNA at K164. PCNA forms a ring-shaped structure consist of homo-trimeric PCNA molecules, which means a single PCNA ring have three modifiable K164. In this study, I investigated the mechanism of DNA damage tolerance pathway which is regulated by simultaneously mono-ubiquitinated PCNA on three K164 in a ring. I analyzed the responses of the cells expressing ectopic PCNA mutated at K164 to DNA damaging agents.
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Free Research Field |
DNA修復
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