2014 Fiscal Year Final Research Report
Physiological roles of TRPM2 in microglial functions
Project/Area Number |
25860172
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
General physiology
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Research Institution | Kyoto Prefectural University of Medicine (2014) Okazaki Research Facilities, National Institutes of Natural Sciences (2013) |
Principal Investigator |
KASHIO Makiko 京都府立医科大学, 医学(系)研究科(研究院), 助教 (20631394)
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Project Period (FY) |
2013-04-01 – 2015-03-31
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Keywords | TRPM2 / レドックスシグナル / 温度 / インスリン |
Outline of Final Research Achievements |
Pancreatic b-cells secrete hypoglycemic insulin upon blood glucose elevation to keep its concentration in the range of physiological levels. Insulin secretion from pancreatic b-cell is well known to be mediated by KATP channel-dependent canonical pathway in which KATP channel closure by intracellular ATP elevation causes membrane depolarization and activation of voltage-dependent Ca channel. However, beside the canonical pathway, KATP channel-independet pathways are recently elucidated to be involved in insulin secretion. As one of them, we have clarified the involvement of TRPM2 function in insulin secretion focusing on redox signal-mediated TRPM2-sensitization leading its activation at body temperature.
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Free Research Field |
生理学
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