| Project/Area Number |
22510212
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Medical genome science
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| Research Institution | Akita University (2011-2013)
Jichi Medical University (2010) |
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Principal Investigator |
IKEDA TAMAKO 秋田大学, 学内共同利用施設等, 助教 (10406035)
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| Co-Investigator(Renkei-kenkyūsha) |
HANAZONO Yutaka 自治医科大学, 医学部, 教授 (70251246)
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| Project Period (FY) |
2010-04-01 – 2013-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ERas遺伝子 / Rho/ROCK経路 / アポトーシス / ROCK阻害薬 / ES細胞 / RHO/ROCK経路 / Rock阻害薬 |
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| Research Abstract |
ERas promotes proliferation of mouse embryonic stem cells, however human ES cells hardly express the ERas gene. Human ES cells , poor survival after cell dissociation is a major obstacle to research, hindering manipulation such as sorting and cloning of cells. On the other hand, treatment of hES cells with ROCK inhibitor markedly diminished apoptosis, enabling hES cells to propagate as mouse ES cells do following dissociation(Watanabe et al.,2007). We examined the relationship between ERas and the Rho/ROCK pathway. Results, our study have revealed a previously unknown pathway that inactivated the Rho/ROCK pathway in ES cells to suppress apotheosis.
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