| Project/Area Number |
26670471
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Hematology
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| Research Institution | Kyushu University |
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Principal Investigator |
ARAI FUMIO 九州大学, 医学(系)研究科(研究院), 教授 (90365403)
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| Research Collaborator |
MacArthur Ben D. 英国、サウサンプトン大学
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 造血幹細胞 / 自己複製 / 細胞分裂 / 自己複製分裂 / Angpt1 / Bmi1 / 老化 / 人工神経回路 / 対称分裂 / 非対称分裂 |
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| Outline of Final Research Achievements |
The number of hematopoietic stem cells (HSCs) is controlled by the balance of the asymmetric/symmetric divisions. We have identified that niche factor Angpt1 increases the symmetric gene expression in paired daughter cells (PDCs) and induces self-renewal division of HSCs. To clarify the function of Angpt1 in the regulation of self-renewal division, we are investigating the function of Bmi1 that is induced symmetric expression between daughter cell pairs by Angpt1 in the regulation of self-renewal of HSCs.
In this study, we also analyzed whether Angpt1 could induce the deterministic HSC self-renewal. We identified that Angpt1-induced self-renewal fitted to the stochastic model in which individual divisions were not closely regulated, regulation was exerted at the level of probabilities. We also analyzed the effect of Angpt1 on cell division induced HSC aging. We found that the culture induced age-related phenotype in PDCs and Angpt1 prevented the cell division induced aging of HSCs.
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