| Project/Area Number |
22710053
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Kyoto University |
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Principal Investigator |
KATO Akihiro 京都大学, 放射線生物研究センター, 研究員 (70423051)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | DNA修復 / 相同組換え / ゲノム / 放射線 / 蛋白質 / 核酸 / 細胞・組織 |
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| Research Abstract |
In order to clarify the biological significance of the physical interaction between NBS1 and RAD51, we tried to establish a NBS1 mutant that was not able to bind to RAD51. In this process, we found that NBS1 interacted with RAD51 through MRE11. The MRE11 mutant that could not interact with RAD51 had full activity of homology-dependent repair of DNA double-strand breaks(DSBs). Cells expressing the MRE11 mutant did not show sensitivity to ionizing radiation. These results indicate that the interaction between NBS1 and RAD51 does not have an important role in DSB repair but has a role in other mechanisms.
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