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
Delayed rectifier K+ current in rabbit atrial myocytes
TL;DR: The role of delayed rectifier K+ current (IK) in rabbit left atrium was examined by applying the whole cell voltage-clamp technique to isolated single myocytes and the IK,tail was almost abolished in most cells by the application of 1 microM E-4031, a class III antiarrhythmic drug.
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A Novel Opener of Large-Conductance Ca2+-Activated K+ (BK) Channel Reduces Ischemic Injury in Rat Cardiac Myocytes by Activating Mitochondrial KCa Channel
TL;DR: Approval of 12,14-dichlorodehydroabietic acid (diCl-DHAA) directly opens mitoK(Ca) channels, prevents Ca(2+) influx into matrix, and reduces ischemic injury in cardiac myocytes.
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BK channel activation by NS-1619 is partially mediated by intracellular Ca2+ release in smooth muscle cells of porcine coronary artery.
TL;DR: The results indicate that the opening of BK channels by NS‐1619 at 30 μM, which is the most frequently used concentration of this agent, is partly due to Ca2+ release from caffeine/ryanodine‐sensitive intracellular storage sites but is mainly due to the direct activation of the channels.
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SK4 encodes intermediate conductance Ca2+-activated K+ channels in mouse urinary bladder smooth muscle cells.
TL;DR: The single channel current of intermediate conductance Ca2 +-activated K+ channel (IK channel) was measured in mouse urinary bladder myocytes (MBM), and the molecular basis of the channel was suggested to be the SK4 subtype by RT-PCR.
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Loss of Transient Receptor Potential Melastatin 3 ion channel function in natural killer cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients
Hélène Cabanas,Katsuhiko Muraki,Natalie Eaton,Cassandra Balinas,Donald Staines,Sonya Marshall-Gradisnik +5 more
TL;DR: TRPM3 activity is impaired in CFS/ME patients suggesting changes in intracellular Ca2+ concentration, which may impact NK cellular functions, and is characterised using whole cell patch-clamp techniques.