| Project/Area Number |
25870691
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cell biology
Biological pharmacy
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| Research Institution | Kyoto Prefectural University of Medicine (2014-2015)
Teikyo Heisei University (2013) |
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Principal Investigator |
Matsuo Kazuhiko 京都府立医科大学, 医学(系)研究科(研究院), 助教 (70599753)
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| Research Collaborator |
TAKAHASHI Mikiko 帝京平成大学, 薬学部, 教授
OHSUMI Keita 名古屋大学, 大学院理学研究科, 教授
SUZAKI Toshinobu 神戸大学, 大学院理学研究科, 准教授
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 中心体 / 中心体複製 / 細胞周期 / 中心体周期 / 中心小体複製 |
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| Outline of Final Research Achievements |
In this study I got following three results which indicated that kendrin and Cep152 may regulate the centrosome duplication. At first, kendrin and Cep152 can interact via their carboxyl terminals. Second, although Cep152 may not localize at the centrosome during G2/M phase they were recruited to the centrosome again during cytokinesis. Third, by siRNA mediated- kendrin depletion, expression level of Cep152 were increased and Cep152 could localize at the centrosome efficiently rather than normal condition. Taken together I found that Cep152 might be recruited efficiently to the centrosome after kendrin was released and that this mechanism could facilitate centrosome duplication at next cell cycle.
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