| Project/Area Number |
12670042
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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 | Saga Medical School |
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Principal Investigator |
YANAGI(ISHIHARA) Faclty of Medicine, Saga Medical School, Associate Professor, 医学部, 助教授 (70265990)
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| Co-Investigator(Kenkyū-buntansha) |
EHARA Tsuguhisa Faculty of Medicine, Saga Medical School, Professor, 医学部, 教授 (50037446)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Potassium channel / Inward rectifier potassium current / Cardiac myocyte |
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| Research Abstract |
The inward rectifier potassium (Kir) channels play an important role in maintaining the resting potential, promoting the repolarization of action potentials and controlling the cell excitability in cardiac myocytes. Kir genes in the subgroup Kir2 encode the a subunits of Kir channels that display the properties of the strong inward rectifier I_<K1> in cardiac myocytes. To explore the significance of different Kir channels in the cardiac function, we studied the electrophysiological properties of the Kir2.1 and Kir2.2 channels of the mouse and human by heterologously expressing them in mammalian cells. We found that Kir2.1 and Kir2.2 channels showed different sensitivities to the blockage by intracellular polyamines and Mg^<2+>, which function as the intrinsic Kir channel blockers. The results suggested that Kir2.1 channel underlies I_<K1> in cardiac myocytes at physiological cytoplasmic conditions. We also studied the function of the human Kir2.1 and Kir2.2 genes cloned from healthy individuals, and found a variance in the Kir2.2 gene, which caused a functional loss of the channel.
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