| Project/Area Number |
16K18992
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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 |
General physiology
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| Research Institution | Keio University |
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Principal Investigator |
YAMAZAKI OSAMU 慶應義塾大学, 医学部(信濃町), 助教 (80757229)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 重炭酸 / トランスポーター / チャネル / リン酸化・脱リン酸化 / 細胞内塩素イオン濃度 / ナトリウム重炭酸共輸送体 / IP3受容体結合蛋白IRBIT / 膵外分泌 / リン酸化部位 / 塩素イオン感知部位 / 重炭酸輸送 / 膵生理 / カルシウムシグナリング / 生理学 / 生理活性 / 内科 |
|---|
| Outline of Final Research Achievements |
Pancreatic excretion system contributes not only digestive systems but also keeping homeostasis. These system deficiency leads to pancreatitis, multiple organ failure, and pancreatic tumor progression.
Here we focused on IP3 receptor binding protein (IRBIT) and calcineurin. These protein acts as a master regulator of pancreatic excretion system, especially for sodium-bicarbonate co-transporter (NBCe1). Novel phosphorylation and dephosphorylation sites in NBCe1 coordinate to IRBIT and calcineurin, leads to fully activation of NBCe1 and bicarbonate excretion.
We submit these novel findings and there are revised in Science Signaling paper.
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