| Project/Area Number |
11470039
|
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | The University of Tokyo |
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Principal Investigator |
AKIYAMA Testu Institute of Molecular and Cellular Biosciences, The University of Tokyo Professor, 分子細胞生物学研究所, 教授 (70150745)
|
|---|
| Project Period (FY) |
1999 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2000: ¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 1999: ¥9,100,000 (Direct Cost: ¥9,100,000)
|
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| Keywords | NMDA receptor / Tumor suppressor / APC / PSD-95 / SPAL / synapse / post synaptic density / learning / 神経 / 海馬 / NMAD受容体 / DLG |
|---|
| Research Abstract |
The synaptic protein PSD95/SAP90 interacts with ion channels such as the N-methyl-D-aspartate-receptor (NMDA-R) via its PDZ domain, and is involved in their clustering. Moreover, it interacts with signaling molecules and plays an important role in coupling NMDA-R to pathways that control synaptic plasticity and learning. We found that PSD-95 is associated with the adenomatous polyposis coli (APC) tumor suppressor protein, Rap1-specific GAP (SPAL), LGN and tyrosine kinase Fyn. Our findings raise the possibility that these molecules are involved in the regulation of NMDA-R clustering and/or NMDA-R-mediated signal transduction.
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