K
Katsuhiko Muraki
Researcher at Aichi Gakuin University
Publications - 120
Citations - 5602
Katsuhiko Muraki is an academic researcher from Aichi Gakuin University. The author has contributed to research in topics: Transient receptor potential channel & Depolarization. The author has an hindex of 37, co-authored 115 publications receiving 4790 citations. Previous affiliations of Katsuhiko Muraki include University of Leeds & Kyoto Prefectural University of Medicine.
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Journal ArticleDOI
Conserved Smooth Muscle Contractility and Blood Pressure Increase in Response to High-Salt Diet in Mice Lacking the β3 Subunit of the Voltage-Dependent Calcium Channel
Manabu Murakami,Hisao Yamamura,Agnieszka Murakami,Tadashi Okamura,Kazuo Nunoki,Minori Mitui-Saito,Katsuhiko Muraki,Takuzou Hano,Yuji Imaizumi,Veit Flockerzi,Teruyuki Yanagisawa +10 more
TL;DR: This work has analyzed beta3-null mice and found that the existence of dihydropyridine (DHP)-sensitive mice show elevated blood pressure in response to a high-salt diet, with significant reductions in plasma catecholamine concentrations.
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Na+ entry through heteromeric TRPC4/C1 channels mediates (−)Englerin A-induced cytotoxicity in synovial sarcoma cells
Katsuhiko Muraki,Kaori Ohnishi,Akiho Takezawa,Hiroka Suzuki,Noriyuki Hatano,Yukiko Muraki,Nurasyikin Hamzah,Richard Foster,Herbert Waldmann,Peter Nussbaumer,Mathias Christmann,Robin S. Bon,David J. Beech +12 more
TL;DR: It is concluded that EA has a potent cytotoxic effect on human synovial sarcoma cells which is mediated by heteromeric TRPC4/C1 channels and Na+ loading.
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Stimulation of human TRPA1 channels by clinical concentrations of the antirheumatic drug auranofin
TL;DR: The study shows that AUR is a potent stimulator of TRPA1 channels, which are highly expressed in sensory neurons as nociceptors and effectively activated TRPA 1 channels expressed in human differentiated neuroblastoma cell lines.
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Molecular Mechanisms for Large Conductance Ca2+-Activated K+ Channel Activation by a Novel Opener, 12,14-Dichlorodehydroabietic Acid
TL;DR: K channel activity was significantly enhanced by diCl-DHAA at concentrations of 0.1 μM and higher in a concentration-dependent manner and kinetic analysis of single channel currents indicates that diCl -DHAA opens BKα mainly by decreasing the time staying in a long closed state.
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Levcromakalim causes indirect endothelial hyperpolarization via a myo-endothelial pathway.
TL;DR: Although RMAECs themselves are functionally insensitive to Levcromakalim, those in an arterial segment are hyperpolarized by levcromkalim via myo‐endothelial electrical communication.