| Project/Area Number |
21770150
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional biochemistry
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
INOUE Hiroki Tokyo University of Pharmacy and Life Science, 生命科学部, 講師 (10294448)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 膜輸送と輸送タンパク質 / 膜輸送 / 細胞骨格 / エンドサイトーシス / ホスホリパーゼA1 / Arf G protein / Rab G protein / WAVE複合体 |
|---|
| Research Abstract |
ASAP1 and FIP3 are effectors and/or regulators of Arf and Rab small G proteins. In this study, the possibility that they are involved in actin cytoskeleton regulation and endocytosis of growth factor receptor was evaluated. For the purpose of this, circular dorsal ruffles formation and PDGF receptor endocytosis was used as a model system. ASAP1 has been proposed to be a negative regulator for CDR formation because its overexpression down -regulates CDR formation. In this work, FI P3, which is an ASAP1-interacting protein, was identified as a positive regulator for CDR formation and PDGF endocytosis. Some of Arf and Rab proteins were localized in CDRs. Taken together, FIP3 may play a role in a crosstalk between actin remodeling and receptor endocytosis as one of key molecules.
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