| Project/Area Number |
26460369
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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 |
General medical chemistry
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| Research Institution | Tokyo Institute of Technology (2015-2017)
Hiroshima University (2014) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SAEKI Yasushi 東京都医学総合研究所, 蛋白質代謝研究室, 副参事研究員 (80462779)
ITO Akihiro 東京薬科大学, 生命科学部, 教授 (40391859)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | インスリン / インスリン様成長因子 / インスリン受容体基質 / ユビキチン / がん / 糖尿病 |
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| Outline of Final Research Achievements |
Insulin plays central roles in the regulation of glucose metabolism. Upon overnutrition, insulin target cells become resistant to insulin, and excessive resistance causes diabetes. Insulin-like growth factor (IGF) is a peptide similar in structure to insulin, and promotes body growth. Excessive sensitivity of cells to IGF contributes to hyper-proliferation and oncogenic transformation of cells. The mechanisms by which the responsiveness of cells to insulin/IGF is altered are not fully understood. In this study, we investigated intracellular signaling that is activated just after insulin/IGF binds to their membrane receptors. We found that IRS2, one of major insulin/IGF signal transducer proteins, associates with a protein called Nedd4. Our study indicated that the excessive disassembly of this Nedd4-IRS2 complex leads to insulin resistance and diabetes, whereas the excessive assembly contributes to hyper-proliferation of cancer cells.
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