Toward understanding the glucose- -cells from analysis of glucose-responsive MafA kinase
Project/Area Number |
22590982
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Metabolomics
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Research Institution | Nara Institute of Science and Technology |
Principal Investigator |
KATAOKA Kohsuke 奈良先端科学技術大学院大学, バイオサイエンス研究科, 准教授 (20262074)
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Project Period (FY) |
2010 – 2012
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Project Status |
Completed (Fiscal Year 2012)
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Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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Keywords | エネルギー・糖質代謝異常・細胞内シグナル伝達・遺伝子発現制御 / タンパク質リン酸化 / 遺伝子発現調節 / 糖尿病 / 細胞内局在 / タンパク質 / リン酸化 / 遺伝子発現制御 / インスリン / 転写調節因子複合体 |
Research Abstract |
We have found that multiple phosphorylation events on MafA transcription factor by GSK3 and MaCK are required for its function in β-cells through enhancing DNA-binding and Beta2 association. Furthermore, We demonstrated that decreased MafA phosphorylation is one of the main causes of β-cell dysfunction in type II diabetes. We also identified a small molecule inhibitor that mimics endogenous MafA de-phosphorylation in β-cells. These findings led to understanding of molecular mechanisms of β-cell function and dysfunction.
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Report
(4 results)
Research Products
(12 results)
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[Journal Article] Insulin transactivator MafA regulates intra-thymic expression of insulin and affects susceptibility to type I diabetes2010
Author(s)
Noso, S., K. Kataoka, Y. Kawabata, N. Babaya, Y. Hiromine, K. Yamaji, Y. Fujisawa, S. Aramata, T. Kudo, S. Takahashi, and H. Ikegami
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Journal Title
Diabetes
Volume: 59
Pages: 2579-2587
Related Report
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