| Project/Area Number |
26550025
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Risk sciences of radiation and chemicals
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| Research Institution | Kyoto University |
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Principal Investigator |
Komatsu Kenshi 京都大学, 放射線生物研究センター, 研究員 (80124577)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 相同組換え修復 / 非相同末端再結合 / 細胞生存曲線の肩 / saturated repair model / DNA修復 / 放射線 / Saturated repair model |
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| Outline of Final Research Achievements |
Present results confirmed the saturation of DNA repair by using the reporter genes, in which the homologous recombination repair functions within a limited region at a low dose. In contrast, non-homologous end-joining has constant activity irrespective of the radiation dose. As a result, the cells exposed to a low dose can survive due to both functional repair pathways: homologous recombination and non-homologous end-joining, while non-homologous end-joining is sole repair pathway at a higher dose. Thus, biological model based on repair activity of cells became plausible to explain the quasi-threshold of radiation survival curve.
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