| Project/Area Number |
26870335
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cell biology
General anatomy (including histology/embryology)
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| Research Institution | Osaka University |
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Principal Investigator |
KUNII MASATAKA 大阪大学, 医学(系)研究科(研究院), 助教 (80614768)
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| Co-Investigator(Renkei-kenkyūsha) |
HARADA Akihiro 大阪大学, 大学院医学系研究科, 教授 (40251441)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | SNARE蛋白質 / SNAP23 / 開口放出 / インスリン分泌 / 神経発生 |
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| Outline of Final Research Achievements |
To elucidate the in vivo function of SNAP23, a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) molecule, we generated central nervous system (CNS)- or pancreatic endocrine-specific SNAP23 knockout (KO) mice.
The CNS-specific KO mice showed severe hypoplasia of cerebral cortex and cerebellum. These results suggest that SNAP23 is essential for brain development.
In the pancreatic endocrine-specific KO mice, pancreatic islets were morphologically normal, but the KO mice showed increased fusion of insulin granules and improved glucose tolerance. These results suggest that SNAP23 has inhibitory role in secretion in the endocrine pancreas.
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