| Project/Area Number |
08458233
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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 |
Cell biology
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| Research Institution | Japanese Foundation for Cancer Research |
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Principal Investigator |
MIYAZONO Kohei The Cancer Institute, Department of Biochemistry, Chief, 癌研究所生化学部, 部長 (90209908)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Mitsuyasu The Cancer Institute, Dept.Biochemistry, Researcher, 癌研究所生化学部, 研究員 (20194855)
ICHIJO Hidenori The Cancer Institute, Dept.Biochemistry, Researcher, 癌研究所生化学部, 研究員 (00242206)
KAWABATA Masahiro The Cancer Institute, Dept.Biochemistry, Researcher, 癌研究所生化学部, 研究員 (60224838)
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| Project Period (FY) |
1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1996: ¥6,300,000 (Direct Cost: ¥6,300,000)
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| Keywords | TGF-beta / activin / bone morphogenetic protein / receptor / signal transduction / serine / threonine kinase / angiogenesis / keratinocyte |
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| Research Abstract |
(1) Identification of GDF-5 receptors : We studied the receptors for growth/differentiation factor-5 (GDF-5), a new member in the bone morphogenetic proteins (BMPs). Although BMP-2 and BMP-7 bind to two different BMP type I receptors (BMPR-IA and BMPR-IB), GDF-5 preferentially bound to BMPR-IB,and only very weakly to BMPR-IA.
(2) Angiogenic activity of GDF-5 : We have found that GDF-5, but not BMP-2, induced angiogenesis in vivo. In in vitro assays using bovine aortic endothelial cells, GDF-5 induced chemotaxis and production of plasminogen activator by the cells.
(3) Differentiation of keratinocytes by activin : We have shown that human epidermal keratinocytes express activin type II and type IB receptors both in vivo and in vitro. Activin induced differentiation of keratinocytes in vitro, but growth inhibitory activity of activin was weak. In contrast, TGF-beta inhibited the growth of keratinocytes, and it did not induce differentiation. Among the Smad family of TGF-beta signal transducers, actvin preferentially activated Smad3, while TGF-beta activated Smad2, Smad3 and Smad4.
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