| Project/Area Number |
10557102
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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 | 展開研究 |
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| Research Field |
Metabolomics
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| Research Institution | Gunma University |
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Principal Investigator |
SHIBATA Hiroshi Institute for Molecular and Cellular Regulation, Gunma University, Department of Cell Biology, Associate Professor, 生体調節研究所, 助教授 (20235584)
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| Co-Investigator(Kenkyū-buntansha) |
KOJIMA Itaru Institute for Molecular and Cellular Regulation, Gunma University, Department of Cell Biology, Professor, 生体調節研究所, 教授 (60143492)
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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 |
¥8,700,000 (Direct Cost: ¥8,700,000)
Fiscal Year 1999: ¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥5,500,000 (Direct Cost: ¥5,500,000)
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| Keywords | insulin / glucose transporter / GTP-binding protein / Rab4 / syntaxin4 / SNARE / ダイナミン |
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| Research Abstract |
In the present study, we investigated the interaction of Rab4 with syntaxin4, a t-SNARE protein implicated in the insulin-induced exocytic fusion of the GLUT4-containing vesicle with the plasma membrane.Rab4 and syntaxin4 were co-immunoprecipitated from the lysates of rat adipocytes. The interaction of the two proteins were attenuated by pretreatment of the cells with insulin but enhanced with GTPγS. A GTPase deficient mutant of Rab4, but not a GTP-binding defective mutant was bound to syntaxin 4, suggesting that the interaction between the two proteins were regulated by the guanine-nucleotide-binding state of Rab4. In addition, we found that the presence of munc-18c, a negative regulator of the SNARE comple formation, displaced Rab4 from syntaxin 4, indicating that the dissociation of munc-18c from syntaxin4 is required for Rab4 to bind to syntaxin 4.
We also clarified that the actin filaments plays a critical role in exocytotic recruitment but not in endocytosis of GLUT4 in isolated rat adipocytes.
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