| Project/Area Number |
04454272
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kansai Medical University |
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Principal Investigator |
INADA Mitsuo Kansai Medical University, Professor of Medicine, 医学部, 教授 (90115791)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUBARA Hiroaki Kansai Medical University, Assistant Professor, 医学部, 助手 (10239072)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1992: ¥5,400,000 (Direct Cost: ¥5,400,000)
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| Keywords | potassium channel / heart / gene / voltage sensitive K^+ channel / 電位依存性カリウムチャネル / 遅延整流型カリウムチャネル / 心筋 / 分子生物学 |
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| Research Abstract |
The regulation of cardiac K^+ channel was examined in Kv1.5 and Kv1.4 genes, known as major K^+ channel in the heart. The genomic clone encoding Kv1.5 was cloned and promoter analysis was performed.There is a cAMP responsive element in the 5'-flanking region. The addition of cAMP analog increased Kv1.5 mRNA levels, but not Kv1.4 mRNA.The run-off assay and gel shift assy demonstrated that this induction is exerted on the gene transcription level. Kv1.4 mRNA levels were regulated by the increase in intracellular Ca^<2+> level and activation of protein kinase C.The myocardial hypertrophy, in which a plateau phase of action potential is reportedly elongated, causes the remarkable repression in Kv1.5 mRNA and significant increase in Kv1.4 mRNA.Thus, although both Kv1.5 and Kv1.4 genes belong to the Shaker K^+ channel family, the regulation of the gene was distinct each other, suggesting that the potassium channel assembly can be altered in the pathological state.
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