1997 Fiscal Year Final Research Report Summary
Molecular cell pharmacology on calcium signaling in diseases
| Project/Area Number |
09044285
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Field |
応用薬理学・医療系薬学
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| Research Institution | Mie University |
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Principal Investigator |
TANAKA Toshio Mie University Faculty of medicine, Professor., 医学部, 教授 (00135443)
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| Co-Investigator(Kenkyū-buntansha) |
HAIZMANN C.W. Zurich University, Clinical Chemistry, Professor, 医学部, 教授
INADA Hiroyasu Mie University Faculty of Medicine, Assistant., 医学部, 助手 (90283522)
NAKA Michiko Mie University Faculty of Medicine, Assistant, 医学部, 助手 (10093139)
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| Project Period (FY) |
1997
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| Keywords | Calcium-binding Proteins / S100C / Differential Gene Expression / Ischemic Heart Disease / Hypoxia / Tumor Cell / Genomic Gene |
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| Research Abstract |
Calcium ions as second messengers contorol many biological processes, at least in part, via intreraction with a large number of calcium-binding proteins. These calcium-binding protein families become of majoc interest because of their different expression in each disease.But it has not been reported about relation disease to calcium-binding protein, S100C we first purified. We already cloned cDNA for S100C and decided the first structure of S100C.So we studied about physiological, pharmacological and pathological roles of S100C in diseases.
We found that S100C bound to propranolol and that the concentrations of propranolol for binding with S100C was similar in which propranolol was reported to exert cardioprotective effects. It sugested that S100C might be intracellular target molecule of propranolol and share other actions than beta-blockade action. We also found that the gene expression of S100C was changed in the heart of myocardial infarction model rats and hypoxia-induced model rats. Moreover, we found a unique structure of the porcine S100C gene. This gene conteins hypoxia-inducible factor (HIF-1). Theses results sugest that S100C might have an impotant role in heart disease.and in pathological vascular remodeling. C.W.Heizmann found differential expression of S100C in disease cells and normal cells and we found cell-cycle dependent differential gene expression of S100C.Thus, S100C might be thought to play an important role in many diseases.
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