| Project/Area Number |
08680916
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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 |
Laboratory animal science
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| Research Institution | Japanese Foundation for Cancer Research |
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Principal Investigator |
MINOWA Osamu Japanese Foundation for Cancer Research, Cancer Institute, Department of Cell Biology, Associate Member, 癌研究所・細胞生物部, 研究員 (00181967)
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| Co-Investigator(Kenkyū-buntansha) |
NODA Tesuo Tohoku University, School of Medicine, Professor, 医学部, 教授 (10183550)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1998: ¥100,000 (Direct Cost: ¥100,000)
Fiscal Year 1997: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1996: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Gene Targeting / CNS Architecture / Tetraploid aggregation / HGF / SF / Aggregation Chimera / 中枢神経系の構築 / 標的遺伝子組換えPCP2遺伝子 / 胎盤 / 4倍体胚会合法 / 表現型のレスキュー |
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| Research Abstract |
Hepatocyte growth factor/scatter factor (HGF/SF) functions as a mitogen, motogen and morphogen for a variety of cultured cells. The genes for HGF/SF and its receptor (the c-met proto-oncogene product) are expressed in many tissues during the embryonic periods and in the adult. HGF/SF is thought to mediate a signal exchange between the mesenchyme and epithelia during mouse development. The mice embryos with a targeted disruption of the HGF/SF gene have severely impaired placentas with markedly reduced numbers of labyrinthine trophoblast cells, and die before birth. The growth of trophoblast cells was stimulated by HGF/SF in vitro, and the HGF/SF activity was released by allantois in primary culture of normal but not mutant embryos. These observations show that HGF/SF is an essential mediator of allantoic mesenchyme-trophoblastic epithelia interaction required for placental organogenesis. To investigate further role for HGF in later stage of development of central nervous system (CNS) architecture, the placental defect of the mutant embryos was rescued by tetraploid aggregation methodology. Using these rescued mutants, histological analysis of CNS are under investigation.
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