Relationship between islet b-cell failure and phosphorylation of b-cell specific transcription factor MafA
| Project/Area Number |
25461353
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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 |
Metabolomics
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| Research Institution | Yokohama City University |
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Principal Investigator |
Kataoka Kohsuke 横浜市立大学, 生命医科学研究科, 准教授 (20262074)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 糖尿病 / 細胞内シグナル伝達 / 遺伝子発現制御 / 膵β細胞機能不全 / リン酸化 / 転写制御因子 / シグナル伝達 / 遺伝子発現 |
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| Outline of Final Research Achievements |
During progression of type-2 diabetes, pancreatic islet b-cells gradually lose their ability to produce and secrete Insulin in response to high blood glucose. To clarify molecular mechanism of the b-cell failure, I analyzed function and activity of b-cell specific transcription factor MafA in b-cells during diabetes progression.
I found that multiple phosphorylation events on MafA regulates its interaction with Beta2, another important transcriptional regulator of b-cell function. I also found that multiple protein kinases phosphorylate MafA redundantly. In b-cells of type-2 diabetes model mice db/db, intracellular distribution and/or abundance of these kinases change during progression of diabetes. Elucidating the mechanism of regulation of these kinases in b-cells may lead to understanding of b-cell failure and contribute to prevention and treatment of diabetes .
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Report
(4 results)
Research Products
(6 results)
