| Project/Area Number |
24790932
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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 |
Metabolomics
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| Research Institution | Kumamoto University |
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Principal Investigator |
SATO Yoshifumi 熊本大学, 大学院生命科学研究部(医), 助教 (90622598)
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| Research Collaborator |
YAMAGATA Kazuya 熊本大学, 大学院・生命科学研究部, 教授 (70324770)
INOUE Masahiro 大阪府立病院機構大阪府立成人病センター, 生化学部門, 部長 (10342990)
OKAMOTO Shiki 自然科学研究機構生理学研究所, 助教 (40342919)
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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 |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 糖尿病 / 転写因子 / インスリン分泌 / 低酸素 |
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| Research Abstract |
HNF4 alpha, a beta-cell transcriptional factor, is a key molecule for insulin secretion from pancreatic beta-cells. Although we found that HNF4 alpha protein was significantly reduced by hypoxia, its molecular mechanism was unclear so far. In this study, we demonstrated that hypoxia-induced activation of AMPK suppresses HNF4 alpha protein levels not via transcriptional regulation, but via ubiquitin-proteasome pathway mediated degradation in vitro. Further experiments are needed to see whether HNF4 alpha protein might be reduced by hypoxia or AMPK activators in vivo.
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