| Project/Area Number |
15590188
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Kagoshima University |
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Principal Investigator |
KAMEYAMA Masaki Kagoshima University, Graduate school of Medical and Dental Sciences, Professor, 大学院・医歯学総合研究科, 教授 (60150059)
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| Co-Investigator(Kenkyū-buntansha) |
YAZAWA Kazuto Kagoshima University, Graduate school of Medical and Dental Sciences, Assistant Professor, 大学院・医歯学総合研究科, 講師 (90212274)
HAO Li-ying Kagoshima University, Graduate school of Medical and Dental Sciences, Research Associate, 大学院・医歯学総合研究科, 助手 (40311881)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2003: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Ca channels / cardiac myocyte / patch clamp / calmodulin / calpastatin / rundown |
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| Research Abstract |
L-type Ca channels in cardiac tissues are regulated by intracellular factors, such as calmodulin(CaM), CaM kinase II(CaMKII) and calpastatin. In this study, following points are clarified.
1.Domain L of calpatatin is known to activate the Ca channels. In this study, we found that a fragment peptide with amino acid number 54-64 has similar effect, suggesting that this region might be an active site for the interaction with the channel.
2.CaM is known to activate rundown channels. In this study, we found that a mutant CaM lacking all four Ca-binding sites can also activate the rundown channels, suggesting that apoCaM interacts with the channel.
3.CaMKII inhibitors reduce basal activity of the Ca channels, suggesting a certain role of CaMKII in the basal activity of the channel.
4.Inhibitors of CaM suppressed the facilitation and inactivation during Ca overload, while inhibitors of CaMKII had minimal effect. This suggest that CaM plays an major role in the facilitation and inactivation induced by a rise of intracellular Ca.
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