Mechanisms and consequences of plasma membrane damage
Project/Area Number |
17H04045
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General medical chemistry
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Research Institution | Okinawa Institute of Science and Technology Graduate University |
Principal Investigator |
Kono Keiko 沖縄科学技術大学院大学, 膜生物学ユニット, 准教授 (30632723)
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥17,810,000 (Direct Cost: ¥13,700,000、Indirect Cost: ¥4,110,000)
Fiscal Year 2019: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2018: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2017: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
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Keywords | 老化 / がん / 細胞膜修復 / 細胞膜損傷 / 膜損傷 / 細胞周期 / 細胞創傷治癒 / 細胞周期チェックポイント / ストレス応答 / 細胞・組織 |
Outline of Final Research Achievements |
The first cell on earth was composed of genetic materials surrounded by membrane. Therefore, plasma membrane repair is fundamental to life. Although plasma membrane repair is involved in a variety of diseases, underlying mechanisms remained unclear. We found that plasma membrane damage induces activation of the cell cycle checkpoint via the degradation of DNA replication machinery as well as stabilization of cell cycle inhibitors. Severer plasma membrane damage contributes to cellular senescence and apoptosis. Normal cells and cancer cells behaved differently after plasma membrane damage. These results may contribute to the development of new cancer therapies in the future.
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Academic Significance and Societal Importance of the Research Achievements |
全ての細胞は膜で囲まれているので、細胞膜の傷を修復する「細胞創傷治癒」は極めて重要です。細胞膜損傷が出来なくなると筋ジストロフィー症など様々な病気になりますが、細胞膜の傷を治す仕組みはまだわからない部分が多く、そのため治療法が見つからない病気がたくさん残っています。本研究により細胞膜を治す過程で細胞が分裂を止める仕組みの詳細が解明されたほか、がん細胞と正常な細胞とで細胞膜が傷ついた時の応答に違いがあることも分かりました。本研究成果をさらに発展させていけば将来的に新たながん治療法の開発につながる可能性があります。
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Report
(4 results)
Research Products
(18 results)
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[Journal Article] Cdk1-mediated DIAPH1 phosphorylation maintains metaphase cortical tension and inactivates the spindle assembly checkpoint at anaphase.2019
Author(s)
Nishimura K, Johmura Y, Deguchi K, Jiang Z, Uchida KSK, Suzuki N, Shimada M, Chiba Y, Hirota T, Yoshimura SH, Kono K, Nakanishi M.
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Journal Title
Nature Communications
Volume: 10
Issue: 1
Pages: 1-10
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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