| Project/Area Number |
23500437
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Gunma University |
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Principal Investigator |
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | タンパク質チロシンリン酸化 / 脳 / ストレス / 神経細胞 / シグナル伝達 / 行動 / 神経科学 / 脳・神経 |
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| Outline of Final Research Achievements |
Forced swim stress induced tyrosine phosphorylation of SIRPα, a membrane protein, in the brain of mice, and the lack of this molecule resulted in increased immobility of mice during forced swim in water. We have published our findings suggesting that the tyrosine phosphorylation of SIRPα in the brain primarily depended on the hypothermia induced by the immersion of mice in cold water. We have also found multiple src family tyrosine kinases participated in the hypothermia-dependent phosphorylation of SIRPα. We found that forced swim stress also induced changes in the phosphorylation level of other signaling molecules, CaMKII, MEK, and CREB. Hypothermia is important for the change of the phosphorylation of CaMKII, but not for MEK and CREB. We also found that a protein phosphatase Shp2, a down-stream signaling molecule of SIRPα, positively regulates tyrosine phosphorylation of SIRPα in the brain, by the use of neuron-specific conditional Shp2 knockout mice.
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