| Project/Area Number |
01044079
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Institution | Kyoto University |
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Principal Investigator |
NUMA Shosaku Kyoto University Faculty of Medicine, 医学部, 教授 (50025516)
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| Co-Investigator(Kenkyū-buntansha) |
KONNO Takashi Max-Planck-Institut fur medizinische Forschung Abteilung Zellphysiologie, プランク医学研究所・細胞生理学部門, 研究員
SAKMANN Bert Max-Planck-Institut fur medizinische Forschung Abteilung Zellphysiologie, プランク医学研究所・細胞生理学部門, 部長
FUKUDA Kazuhiko Kyoto University Faculty of Medicine, 医学部, 助手 (90199224)
TANABE Tsutomu Kyoto University Faculty of Medicine, 医学部, 助手 (70183069)
IMOTO Keiji Kyoto University Faculty of Medicine, 医学部, 講師 (00176512)
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| Project Period (FY) |
1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥7,300,000 (Direct Cost: ¥7,300,000)
Fiscal Year 1989: ¥7,300,000 (Direct Cost: ¥7,300,000)
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| Keywords | Nicotinic acetylcholine receptor / Sodium channel / Calcium channel / Site-directed mutagenesis / cDNA expression / Patch-clamp / Voltage sensor / Tetrodotoxin |
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| Research Abstract |
Neurotransmitter receptors and ionic channels are membrane proteins essential for neural signalling. Cloning and sequencing of cDNAs have revealed the primary structures of different families of receptors and channels. The structural basis for the function of neurotransmitter receptors and ionic channels has been investigated by the combined use of molecular-biological and electrophysiological methods. Thus receptor and channel proteins and their mutants have been produced by expression of the respective cDNAs, and the functional properties of the wild-type and mutant proteins have been analysed. The main findings obtained concern the identification of a channel-forming region of the nicotinic acetylcholine receptor, the identification of a voltage sensor segment responsible for activation of the sodium channel and the functional role of the skeletal muscle slow calcium channel in excitation-contraction coupling.
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