2023 Fiscal Year Final Research Report
TRIC and MG23 channels in store Ca2+ handling
| Project/Area Number |
21H02663
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 48020:Physiology-related
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | Ca2+ストア / 小胞体 / イオンチャネル |
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| Outline of Final Research Achievements |
Tric-b-knockout mice provide an animal model of osteogenesis imperfecta. We found atypical cell death in Tric-b-knockout growth plate chondrocytes, that is caused by hyperactivation of the ER stress sensor PERK. In the muscle skinned fiber preparations from Mg23-knockout mice, we detected altered store Ca2+ handling, that is likely caused by insufficient Ca2+ leakage. Our observations indicate that TRIC and MG23 channels function as cation channels in sarco/endoplasmic reticulum and physiologically contribute to store Ca2+ handling.
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| Free Research Field |
細胞生理学
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| Academic Significance and Societal Importance of the Research Achievements |
小胞体Ca2+ストアは細胞機能に不可欠であり、様々な細胞応答を制御する。一方で、Ca2+ストアのイオンバランスの分子機序は未開拓な学術分野であり、その疾患病態との関連も不明である。当研究遂行による成果は、TRICおよびMG23チャネルのイオン透過性はCa2+ストア機能維持に不可欠であることを示し、TRIC-B欠損による骨形成不全症の発症メカニズムの解明に貢献した。
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