| Project/Area Number |
16K00544
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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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 |
IKURA MASAE 京都大学, 生命科学研究科, 研究員 (40535275)
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| Research Collaborator |
MATSUDA tomonari
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | DNA損傷応答 / アセチル化 / TRRAP / ATM / TIP60 |
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| Outline of Final Research Achievements |
We have already shown that TIP60 histone acetyltransferase complex regulates H2AX exchange via its acetylation at DNA damage sites. However, it remains unclear how this acetylation is maintained and facilitated at DNA damage sites. In this study, focusing on the component of TIP60 complex, TRRAP, we found that TRRAP recruits TIP60 to DNA damage sites and regulates acetylation-dependent H2AX exchange. Since it is known that TRRAP is a member of PI3 kinase family but has no kinase activity, it is predicted that TRRAP competes against ATM in a DNA damage response.However, our study demonstrated that TRRAP and ATM do not compete each other, but have distinct roles in DNA damage response under the circumstances of different radiation dose rate.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の研究で、ヒストンH2AXのアセチル化の放射線ストレス応答における役割の一端が、明らかになった。アセチル化の責任酵素であるTIP60複合体の構成因子であるTRRAPに着目したことによって、H2AXのアセチル化とリン酸化の関係は、異なる線量率によってそれぞれその役割が異なることが見えてきた。これらの知見は、、福島原発事故の生体に対する放射線影響の分子レベルでの理解に貢献できると考えられる。
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