2016 Fiscal Year Final Research Report
Identification and dissection of ATR substrates
Project/Area Number |
25701005
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Research Category |
Grant-in-Aid for Young Scientists (A)
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Allocation Type | Partial Multi-year Fund |
Research Field |
Risk sciences of radiation and chemicals
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Research Institution | National Cancer Center Japan (2014-2016) Hiroshima University (2013) |
Principal Investigator |
Shiotani Bunsyo 国立研究開発法人国立がん研究センター, 研究所, 主任研究員 (10627665)
|
Project Period (FY) |
2013-04-01 – 2017-03-31
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Keywords | ATR / DNA損傷応答 / DNA複製ストレス |
Outline of Final Research Achievements |
ATR is a kinase that regulates the DNA damage response and maintains genome stability. ATR has been shown to respond to a wider range of DNA damage and exhibit diverse functions. In this study, we aimed to clarify the mechanism underlying DNA structure-dependent activation of ATR and to identify the direct substrate of ATR. As a result, we found a novel ATR activation mechanism at the DNA double strand break site. We also made analog susceptible ATR mutants and successfully detected and identified many unknown substrates.
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Free Research Field |
DNA損傷応答
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