| Project/Area Number |
01580153
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
物質生物化学
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| Research Institution | University of Tokyo |
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Principal Investigator |
TSUJI Shuichi University of Tokyo, Faculty of Medicine, ASSISTANT, 医学部(医), 助手 (90124677)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1990: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1989: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Ganglioside / Protein phosphorylation / Cell surface / Neuroblastoma cell line / ecto-type protein kinase / Neuritogenesis / ガングリオシド / 神経突起伸展作用 / 神経膠腫細胞 |
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| Research Abstract |
Gangliosides are known as several cellular markers and receptors for some biofactors, and also known as the modulators of protein kinases including ecto-type protein phosphorylation. Recently we found that GQ1b can specifically promote neuritogenesis of the human neutoblastoma cells (GOTO) and also that GQ1b specifically stimulates the phosphorylation of several cell surface proteins of the same cells. A protein kinase inhibitor, K-252b which cannot pass through the membrane, inhibit the GQ1b-stimulating phosphorylation. The results indicate that this cell surface protein phosphorylation might be carried out by unique ecto-type protein kinases which is specifically activated by GQ1b. K-252b also inhibited the GQ1b-dependent promotion of neuritogenesis. The GQ1b-dependent stimulation of phosphorylation may be necessary for promoting the neuritogenesis. These results strongly suggest the interrelationship between those two cell events and occurrence of a new biosignal transduction, ecto biosignal transduction system.
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