| Project/Area Number |
09670051
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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 Faculty of Medicine, Kagoshima University, Professor, 医学部, 教授 (60150059)
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| Co-Investigator(Kenkyū-buntansha) |
〓 〓英 鹿児島大学, 医学部, 助手
KAMEYAMA Asako Faculty of Medicine, Kagoshima University, Research Associate, 医学部, 助手 (70244225)
HAO L-Ying Faculty of Medicine Kagoshima University, Research Associate
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Ca channel / calpastatin / patch clamp / cardiac myocytes / 心筋 / カルシウムチャネル |
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| Research Abstract |
Voltage-operated L-type Ca^<2+> channels play important roles in cellular excitation related to rhythmic firing, synaptic transmission, muscle contraction and secretion. However, run-down of the Ca^<2+> channel has been an obstacle to studies of the channel. We have been investigating the mechanism of run-down in relation to the understanding of the regulation of channel activity. We have suggested previously that cytoplasmic factors are involved in maintenance of channel activity, and that wash-out of the factors is the cause of run-down. The properties of one possible factor in cytoplasm resemble those of calpastatin, an endogenous inhibitor of Ca-activated neutral protease. However, fractionated cytoplasm or purified calpastatin shows a limited ability to recover channel activity. This implied that there might be other co-factor(s). Therefore, this study was carried out to elucidate the nature of the cytoplasmic factors. It was found that another protein-like factor, together with calpastatin and ATP, restores L-type Ca^<2+> channel activity.
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