| Project/Area Number |
11558099
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Laboratory animal science
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| Research Institution | RIKEN (THE INSTITUTE OF PHYSICAL AND CHEMICAL RESERCH) (2001)
Osaka University (1999-2000) |
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Principal Investigator |
NIWA Hitoshi RIKEN CENTER FOR DEVELPMENTAL BIOLOGY, LABORATORY FOR PLURIPOTENT CELL STUDIES, TEAM LEADERNETWORK DEVELOPMENT, TEAM LEADER (RESEARCHER), 多能性幹細胞研究チーム, チームリーダー(研究職) (80253730)
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| Co-Investigator(Kenkyū-buntansha) |
宮崎 純一 大阪大学, 医学系研究科, 教授 (10200156)
田代 文 大阪大学, 医学系研究科, 助手 (40136213)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥8,100,000 (Direct Cost: ¥8,100,000)
Fiscal Year 2001: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2000: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1999: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | ES cells / serum / feeder cells / proliferation / インスレーター / 胚性幹細胞 / 遺伝子発現 / 未分化状態 / 発現ライブラリー |
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| Research Abstract |
We found the autocrine activity derived from ES cells to support ES self-renewal in the absence of serum and feeder cells, and named it KSRS. Since we could not identify KSRS by expression cloning and testing known candidates, we tried to purify it from the serum that contains the same activity. Now purification has almost finished and we will analyze the purified fraction by mass-spectrometry.
We have already confirrned that this activity can support self-renewal of 129-derived ES cells by culturing them for 1 week with semi-purified fraction followed by blastocyst injection, resulting formation of chimeric mice. Moreover, this serum-free culture condition allowed propagation of ES cells from C57BL6 blastocysts very efficiently in the presence of feeder cells, so now we are trying to remove feeder cells from this condition by choosing appropriate matrix that allows efficient attachment of blastocysts.
We investigated about the role of TGF-b superfamily on ES cell growth by modulation of Smad signaling pathway. Since Smad7 overexpression repress proliferation of ES cells and this negative effect can be relieved, the Smad signal would has physiological function to stimulate ES cell proliferation.
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