| Project/Area Number |
05670040
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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 |
General physiology
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| Research Institution | Tokyo Medical and Dental University, Medical Research Institute. |
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Principal Investigator |
KAWANO Seiko Tokyo Medical and Dental University, Medical Research Institute, Associate Professor, 難治疾患研究所, 助教授 (00177718)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Sarcoplasmic Reticulum / Ryanodine Receptor / Ca^<2+> / Cl-channel / Cardiac Myocyte / Signal Transduction / リアノジン受容体 / 細胞内Ca^<2+> / クロライドチャネル / 筋小胞体 / Mg^<2+> / イオンチャネル / カルモジュリン / カルシュウム |
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| Research Abstract |
I have investigated the regulatory mechanism of ion channels in cardiac sarcoplasmic reticulum by recording single channel currents.
(1) I found that Cl-channel existed in cardiac sarcoplasmic reticulum (SR) and that this channel was activated by cyclic AMP-dependent phosphorylation and was inhibited by Ca^<2+>/calmodulin complex. These are new evidences of intracellular channel regulations. I published the paper about these evidences (Circulation Research, 1993). (2) Ryanodine receptor Ca^<2+> release channel (RyR) in SR playd the important role for Ca^<2+> supply in the cells. We examined the regulatory mechanisms of RyR by recordingsingle channel activities and found that these channel openings were enhanced by scorpion toxin, which might be the new type of activator for ryanodine receptor. Ca^<2+> antagonist, verapamil, blocked ryanodine receptor channel openings directly to reduce the contraction of the heart. I showed the detail regulatory mechanisms of Ca^<2+> release from SR by Mg^<2+>.
(2) Intracellular Ca^<2+> is supplied from SR and plays many important roles for cell functions. I found that cardiac sarcolemma had Ca^<2+> -activated C1-channel and examined the detail activation mechanisms of this channel by intracellular Ca^<2+>. This paper is now in press of Journal of Physiology in London. I need to study the further regulatory mechanisms of this Cl-channel.
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