Elucidation of growth mechanisms of pancreatic .-cells with new developed procedures
| Project/Area Number |
21689007
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | Gunma University |
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Principal Investigator |
TORII Seiji 群馬大学, 生体調節研究所, 准教授 (40312904)
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| Co-Investigator(Renkei-kenkyūsha) |
YAMADA Keiichi 群馬大学, 工学研究科, 助教 (70323334)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥23,270,000 (Direct Cost: ¥17,900,000、Indirect Cost: ¥5,370,000)
Fiscal Year 2011: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
Fiscal Year 2010: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
Fiscal Year 2009: ¥9,230,000 (Direct Cost: ¥7,100,000、Indirect Cost: ¥2,130,000)
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| Keywords | インスリン / 脱リン酸化酵素 / ペプチドホルモン / 分泌顆粒 / 糖尿病 / オートクライン / 分泌 / 細胞内輸送 / 細胞増殖 / 細胞内輸 |
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| Research Abstract |
Phogrin, a member of receptor protein tyrosine phosphatases, primarily localize on secretory granules (SGs) in a variety of neuroendocrine cells including pancreatic β-cells, and recycle between SGs and the plasma membrane upon stimulation of regulated secretion. We suggest that the transitory interaction of phogrin with insulin receptor enables autocrine insulin action in pancreatic β-cells through stabilization of IRS2 protein by inhibition of negative feedback mechanism. We also suggest that phogrin has a supportive role in SG formation, through providing a communication mechanism between the luminal CPE complex and the cytoplasmic transport machinery.
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Report
(4 results)
Research Products
(29 results)
