| Project/Area Number |
08457616
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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 | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | SHOWA UNIVERSITY |
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Principal Investigator |
SHIBANUMA Motoko Showa University School of Pharmaceutical siences Assistant Professor, 薬学部, 助教授 (60245876)
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| Co-Investigator(Kenkyū-buntansha) |
MASHOMO Junichi Showa University School of Pharmaceutical siences Assistant, 薬学部, 助手 (60054045)
NOSE Kitoshi Showa University School of Pharmaceutical siences Professor, 薬学部, 教授 (70012747)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 1997: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1996: ¥4,100,000 (Direct Cost: ¥4,100,000)
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| Keywords | differentiation / Zn finger protein / HIC-5 / expression vectors / focal adhesion / Alu配列 |
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| Research Abstract |
Roles of the hic-5 gene that encodes a novel Zn-finger protein in cellular differetiation was examined using sense-and antisense-expression vectors for hic-5. Forced expression of sense-strand of hic-5 did not affect the differentiation processes of myogenic C2C12 or osteoblastic RCT-1 cells, but introduction of antisence expression vectors inhibited osteogenic differentiation as revealed by decrease in expression of extracellular matric proteins and alkaline phosphatase. These sffects seemed to be a result of AP-1 activation through constitutive expression of c-fos gene that was caused by the HIC-5.
Immunocytochemical studies using specific antiboby against HIC-5 showed that the protein localize in focal adhesion plaques in normal fibroblasts, and the HIC-5 associates with vinculin, talin and FAK.It was speculated that the HIC-5 protein is a gate keeper for signal transduction pathways from cellular surface to nuclei.
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