| Project/Area Number |
02807034
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | University of Occupational and Environmental Health, School of Medicine |
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Principal Investigator |
HIRANO Hideyasu Univ. Occu. Env. Health ; Dept. Biochemistry, Assistant Prof., 医学部・生化学, 講師 (50040241)
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| Co-Investigator(Kenkyū-buntansha) |
GOTOH Sadao Univ. Occu. Env. Health ; Dept. Biochemistry, Associate Prof., 医学部・生化学, 助教授 (50131917)
HIGASHI Ken Univ. Occu. Env. Health ; Dept. Biochemistry, Professor, 医学部・生化学, 教授 (30028386)
唐崎 裕治 産業医科大学, 医学部・生化学, 助手 (20140907)
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| Project Period (FY) |
1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Fibronectin / Profilin / ECM / Basement membrane / Collagen / Controlling Morphology Proteins / Morphological control / Nephritis / ファイブロネクチン / cDNA / イムノゲノサイト / ネフリトゲノサイド / PCR |
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| Research Abstract |
Fibronectin is an extracellular adhesive protein which actively functions during wound healing, cell migration, phagocytosis of Kupffer's cell or macrophages, etc. Cellular fibronectin promotes the differentiation of the neural crest cells to adrenergic phenotype of cells. Whereas the myotube formation process induced by the fusion of nyoblast was inhibited by fibronectin. This activity indicated that fibronectin is a differentiation inhibition substance. In the case of chondrocyte cell culture, fibronectin causes dedifferentiation of chondrocytes to a phenotype resembling the nesenchynal cell. Thus the fibronectin has inconsistent functions in the molecule. We thought from these published results that fibronectin could be a controlling morphology protein rather than a differentiation or dedifferentiation substance. Our target was to clone controlling morphology proteins, then we had to exclude many metabolic enzymes distributed in the organs(kidney, liver, lung etc.). We investigated
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to obtain or to discover proteins which change morphology, acting outside or beneath the membrane, through nephritis and fibrosis. We used antibodies against kidney basement membranes to obtain clones carrying cell surface vicinal proteins. Several inserts cDNAs obtained by library screenings of lambda-gtll were used as probes for Northern blot hybridization. The probe purified from 21st clone(lambda NH21)showed an increased level of expression through wound-healing/fibrosis. Sequenced NH21 was homologous to human profilin cDNA. Our nobel approach decreased the obtaining possibility of cytoplasmic metabolic enzyme eDNAs, and at the same time, this gave us to identity controlling morphology proteins speedily and to find out a protein links to signal transduction, that is, one of the obtained clones carried profilin cDNA.
The approach using pentapeptide(VIO)which is a part of type III repeat of fibronectin, VIO induced thymocyte differentiation.
We have not yet succeeded by the approach to obtain cDNA coding Nephritogenoside using PCR technique and direct hybridization of synthetic oligos to lambda-gtllcDNA library. Less
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