| Project/Area Number |
23591086
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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 |
Circulatory organs internal medicine
|
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
TETSUJI Miura 札幌医科大学, 医学部, 教授 (90199951)
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| Co-Investigator(Kenkyū-buntansha) |
MIKI Takayuki 札幌医科大学, 医学部, 准教授 (00336405)
TANNO Masaya 札幌医科大学, 医学部, 講師 (00398322)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | ミトコンドリア / 細胞死 / 細胞内情報伝達 / 活性酸素 / 透過性遷移孔 |
|---|
| Research Abstract |
The aim of this study was to characterize roles of protein kinases in regulation of mitochondrial permeability transition pore (mPTP) opening. We found that interaction of cyclophilin D (CypD) and inorganic phosphate carrier (PiC) determines the threshold for mPTP opening and that translocation of GSK-3beta via its interaction with VDAC2 and subsequent interaction with complex III promotes mPTP opening by enhanced production of reactive oxygen species. Inactivation of GSK-3beta by PI3K-Akt signaling or by activation of the mitochondrial KATP channel was found to increase threshold for mPTP opening and also to accelerate re-closure of opened mPTP, leading to protection from cell necrosis.
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