| Project/Area Number |
15K07158
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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 |
Genetics/Chromosome dynamics
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| Research Institution | Tottori University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
中山 祐二 鳥取大学, 生命機能研究支援センター, 助教 (40432603)
古倉 健嗣 鳥取大学, 医学部, 助教 (30344039)
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| Research Collaborator |
Li Yanze
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | SIRT2 / オートファジー / 紡錘体チェックポイント / 細胞死 / 四倍体 / M期停止 / p53 / アポトーシス / 微小核 |
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| Outline of Final Research Achievements |
The action of anti-cancer drug such as microtubule inhibitors targeting spindle assembly checkpoint depends on mitotic cell death and cell death after mitotic slippage. This study focused the latter cell death that has been reported to be involved in basal autophagy level by our study. As a pathway escaping from the cell death, we assumed double mitosis in tetraploid cells, which allows re-diploidization, since surviving cells after mictotuble inhibitors are diploid cells. However, double mitotis were not observed in the tetraploid cells in microtubule inhibitor-resistant cells, thus we newly generated our working hypothesis that abnormally prolonged mitotic arrest observed are due to escape from mitotic cell death. We tried to identify the responsible molecules for the process, whose expression depends on the basal autophagy level. We identified two possible molecules, p53 and apoptosis-regulating molecule A.
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