| Project/Area Number |
16K07343
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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 |
Cell biology
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| Research Institution | Tokyo University of Agriculture and Technology |
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Principal Investigator |
Saito Mikako 東京農工大学, 工学(系)研究科(研究院), 准教授 (20291346)
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| Research Collaborator |
ASAI yuma
TANAKA kento
IMAI keiichi
HIRATOKO shoya
TOKUNAGA naruwa
KISHI ryota
SAITO toshiki
SASAI tomoko
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| Project Period (FY) |
2016-10-21 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | Cx30.3 / コンタクトアクティベーション / マウスES細胞 / 細胞間コミュニケーション / 細胞間情報伝達 / コネキシン |
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| Outline of Final Research Achievements |
In the process of comprehensive analysis of the connexin (Cx) group involved in intercellular molecular signal transduction, it was found that Cx30.3 was expressed only at the adjacent cell-cell contact region in mouse ES cells. In this study, expression analysis was performed at the Cx30.3 gene and protein level. Cx30.3 gene expression was activated in response to cell-cell contact in ES cells. The promoter region of Cx30.3 was determined and the initial process of the intracellular signaling pathway was clarified. In addition, it was observed that Cx30.3 moved to the cell-cell contact region in a short time when the expression of Cx30.3 was analyzed in real time. Cx30.3 might have the new function of recognizing the same type of cell-cell contact.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、Cx30.3が同種の細胞接触情報を細胞内に伝達し発現を増加するという細胞認識機能を有する可能性を示した。これは、異常な細胞が隣接している場合を検知できる可能性を示唆するものであり、多細胞生物の多様な細胞間コミュニケーションの分子機構の解明に向けた重要な知見である。ヒトを含む多細胞生物は、未分化状態の幹細胞から機能細胞への分化を経て、個体を創製し維持している。個々の細胞の性質は異なるが、細胞間のコミュニケーションによって全体として統御された機能を維持していると考えられる。この仕組みを解明することは、恒常性維持および恒常性破綻時の病気発症のメカニズムの解明につながり、その意義は大きい。
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