| Project/Area Number |
08457057
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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
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| Research Institution | Kyorin University school of Medicine |
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Principal Investigator |
NAGAMATSU Shinya Kyorin Univ.Sch.of Med., Dept.of Biochem., Associate Professor, 医学部, 助教授 (80231489)
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| Co-Investigator(Kenkyū-buntansha) |
SAWA Hiroki Kyorin Univ.Sch.of Med., Dept.of Neurosurgery, Assintant Professor, 医学部, 講師 (80135912)
WATANABE Takashi Kyorin Univ.Sch.of Med., Dept.of Clinical Pthology, Associate Professor, 医学部, 助教授 (00191768)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1998: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Syntaxin / SNARE / Exocytosis / Pancreatic beta cell / SNAP / Diabetes Medllirus / Pancreatic βcell / インスリン分泌 / 膵β細胞 / NSF / 調節性分泌機構 / 構成性分泌機構 / 膵β細部 |
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| Research Abstract |
The molecular mechanism of insulin exocytotic process in pancreatic beta cells is still unknown. Recently ; the fundamental components of the machinery for docking/fusion process have been revealed. These components include NSF, SNAP, and SNAP receptors. In the present project, we studied the functional roles of these components in insulin exocytotic process, and further examined the relationship between SNAP receptors and diabetes mellitus. We summarized the points of this research project as follows.
1) Syntaxin lA and SNAP-25 were expressed in pancreatic p cells and the biosynthesis was regulated by glucose.
2) alpha-SNAP plays a crucial role in glucose-stimulated insulin exocytosis via large dense core vesicles, but not GABA release via synaptic-like microvesicles inpancreatic beta cells.
3) alpha-SNAP functions in insulin exocytosis from mature, but not immature insulin secretory granules.
4) Expression of t-SNAREs was decreased in diabetic GK rat islets. Restoration of decreased t-SNARE protein to the normal level improved the impaired insulin release in diabetic GK rat islets.
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