| Project/Area Number |
10671109
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Fukui Medical University |
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Principal Investigator |
YAMAGUCHI Akio Fukui Medical University, First Department of Surgery, Professor, 医学部, 教授 (10174608)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Reps / Ral / RalBPl / small GTPase / RalBP1 / Ra1 / Ra1BP1 / EGFR |
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| Research Abstract |
Ras proteins have the capacity to influence a wide variety of cellular processes, including cell cycle control, induction of differentiation, rearrangement of the actin cytoskelton, and apoptosis. We identify another potential binding partner for RalBP1. This protein has an Eps homology (EH) domain and becomes tyrosine-phosphorylated in response to EGF signaling. RalBP1 associated Eps domain-containing protein (Reps) may mediate an additional function of RalBP1. In addition, Reps has the capacity to form a complex with the SH3 domains of the adapter proteins Crk and Grb2, which may link Reps to an EGF-responsive tyrosine kinase. Reps may coordinate the cellular actions of activated EGF receptors and Ral-GTPase.
And we investigated the contribution of the Ral-GEF signaling pathway to NGF-induced differentiation of PC12cells. Ral-GEF signaling opposed the actions of Raf and PI3 kinase signaling. Constitutive elevation of Ral-GEF activity suppressed neurite outgrowth and cell cycle arrest induced by NGF, whereas constitutive inhibition of Ral-GEF activity enhanced the rate of NGF-induced neurite outgrowth and cell cycle exit.
The ratio of activities among Ras effectors and their temporal regulation may be important determinants for cell fate decision between proliferation and differentiation.
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