| Project/Area Number |
24790311
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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 |
Pathological medical chemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MATSUURA Ken 東京大学, 分子細胞生物学研究所, 助教 (10625742)
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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 |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 神経科学 / てんかん / 自閉症 / シナプス可塑性 |
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| Research Abstract |
SPAL-1 is a neuronal protein abundantly expressed in excitatory synapses. However, its physiological function is poorly understood. We have previously shown that SPAL-1 KO mice exhibit intellectual disabilities and autism-like behaviors, which suggest an important role of SPAL-1 in higher brain function. In this research, we further attempted to elucidate molecular mechanism involving SPAL-1. We performed comprehensive screening of physiological interactants of SPAL-1 in mouse forebrain using IP-MS analysis. SPAL-1 was cross-linked to the adjacent proteins prior to cell lysis to preserve the original complex and avoid artificial binding in the later procedures. Sample from SPAL-1 KO mice was used as negative control. As a result, we have identified several promising interactants such as endocytotic factors and subunits of sodium-potassium pump, that may lead to an elucidation of the molecular function of SPAL-1 in the brain.
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