| Project/Area Number |
24710057
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Tohoku University |
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Principal Investigator |
UI Ayako 東北大学, 加齢医学研究所, 助教 (00469967)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | LKB1 / クロマチンリモデリング / DSB修復 / AMPK2 / SWI/SNF / ATM / SWi/SNF / 細胞がん化 / 癌治療 / DNA二本鎖修復 |
|---|
| Research Abstract |
LKB1 regulates multiple processes by phosphorylating adenosine monophosphate–activated protein kinases (AMPKs). LKB1 and AMPK2 proteins were found here to be recruited to DNA double strand break (DSB) sites. Their depletion or inhibition compromises the ability of cells to repair DNA by non-homologous end joining (NHEJ) by suppressing accumulation of KU70, a key NHEJ protein, and of BRM, a catalytic subunit in the SWI/SNF complex to DSB sites, resulting in the occurrence of chromosome breaks. Histone H2B mutants lacking AMPK2 phoshorylation site impaired the KU70 and BRM recruitment. LKB1-AMPK2 signaling is likely to regulate NHEJ and contribute to genome stability.
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