| Project/Area Number |
16K15672
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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 |
Anesthesiology
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| Research Institution | Yamagata University |
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Principal Investigator |
AKimoto Ryo 山形大学, 医学部, 助教 (40594677)
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| Co-Investigator(Kenkyū-buntansha) |
川前 金幸 山形大学, 医学部, 教授 (70254026)
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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 |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 低酸素 / ジアシルグリセロールキナーゼ / AMPK / SIRT / ゼータ型DGK |
|---|
| Outline of Final Research Achievements |
The expression of AMPKα increased in a time-dependent manner by hypoxic loading in wild type cultured cells. On the other hand, in DGKζ-KO cells, AMPKα already showed high expression levels at normoxic pressure, but gradually decreased due to hypoxic load. Hypoxic stimulation increased expression of active AMPKα. DGKζ-KO cells had higher activation than wild type. However, their control mechanisms have not been elucidated.
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| Academic Significance and Societal Importance of the Research Achievements |
AMPKαを中心とした細胞のエネルギーセンサーの、低酸素環境下で振る舞いを実験的に検討した。これまでDGKζと低酸素負荷との関係の報告は少ないが、今回DGKζが細胞のエネルギー調節に関わっている可能性が示唆され、またDGKζ発現減少細胞は低酸素負荷に脆弱な可能性が考えられた。しかし、その詳細なメカニズムまでは解明に至らなかったが、今後の研究や治療のヒントとなる知見を得られた。
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