Physiological role of KCa1.1 channel in ER membrane
| Project/Area Number |
15K08169
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Research Collaborator |
Maruyama Yoshio
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | イオンチャネル / 小胞体 |
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| Outline of Final Research Achievements |
Ion channels working at plasma membrane are assembled in endoplasmic reticulum, then they are transported to their destination via Golgi apparatus. But it is unclear that whether they are conferred any function(s) and physiological role(s) in the intracellular membrane.
We observed large conductance Ca2+-activated K+ (MaxiK) currents in nuclear envelopes (peri-nuclear ER membrane) of pancreatic acinar cells and HEK293 cells using the patch-clamp technique. Consequently we tried to elucidate role(s) of this channel in ER membrane. We evaluated alteration in free Ca2+ content in the ER expressing MaxiK channel and indicated that MaxiK-expressing HEK293 cells have larger Ca2+ content in ER than wild type HEK293 cells.
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| Academic Significance and Societal Importance of the Research Achievements |
近年、神経疾患や糖尿病、急性膵炎などの疾患に小胞体の機能異常が関与することが明らかになるなど、小胞体の生理的、病理的役割が注目されている。しかし、小胞体内のイオン環境に着目した研究はほとんどない。
本研究では、K+チャネルにより（イオン透過を介さずに）小胞体Ca2+イオン濃度が変化するという現象の発見、ER内pH変化の観察手法の確立などに至った。これらの成果は、ER内のイオン環境研究の端緒となり、小胞体機能のさらなる理解、生理的・病理的役割の解明に繋がるものである。
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Report
(5 results)
Research Products
(6 results)
