The antimalarial agent mefloquine inhibits ATP-sensitive K-channels.
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The role of pannexin hemichannels in the anoxic depolarization of hippocampal pyramidal cellsGap junction blockers: a potential approach to attenuate morphine withdrawal symptoms.Pharmacological stimulation and inhibition of insulin secretion in mouse islets lacking ATP-sensitive K+ channelsSpecific residues of the cytoplasmic domains of cardiac inward rectifier potassium channels are effective antifibrillatory targets.Role of ubiquitin-proteasome degradation pathway in biogenesis efficiency of {beta}-cell ATP-sensitive potassium channels.Anti-malaria drug mefloquine induces motor learning deficits in humansMefloquine induces dose-related neurological effects in a rat model.Utility of alkylaminoquinolinyl methanols as new antimalarial drugs.Safety evaluation of fixed combination piperaquine plus dihydroartemisinin (Artekin) in Cambodian children and adults with malaria.Antimalarial drugs: QT prolongation and cardiac arrhythmias.Complex Membrane Channel Blockade: A Unifying Hypothesis for the Prodromal and Acute Neuropsychiatric Sequelae Resulting from Exposure to the Antimalarial Drug Mefloquine.Adverse effects of mefloquine for the treatment of uncomplicated malaria in Thailand: A pooled analysis of 19, 850 individual patientsMolecular mechanisms of chloroquine inhibition of heterologously expressed Kir6.2/SUR2A channels.Serotonin evokes endocannabinoid release and retrogradely suppresses excitatory synapses.Potent block of Cx36 and Cx50 gap junction channels by mefloquine.Connexin channel modulators and their mechanisms of action.Adverse neuropsychiatric effects of antimalarial drugs.Novel members of quinoline compound family enhance insulin secretion in RIN-5AH beta cells and in rat pancreatic islet microtissue.Formulation and evaluation of Pheroid vesicles containing mefloquine for the treatment of malaria.Inhibitors of connexin and pannexin channels as potential therapeutics.Aberrant connexin26 hemichannels underlying keratitis-ichthyosis-deafness syndrome are potently inhibited by mefloquine.Transcriptomic profiling of the Saccharomyces cerevisiae response to quinine reveals a glucose limitation response attributable to drug-induced inhibition of glucose uptake.Intraglomerular gap junctions enhance interglomerular synchrony in a sparsely connected olfactory bulb network.Reversal of loss of bone mass in old mice treated with mefloquine
P2860
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P2860
The antimalarial agent mefloquine inhibits ATP-sensitive K-channels.
description
2000 nî lūn-bûn
@nan
2000 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2000 թվականի հոտեմբերին հրատարակված գիտական հոդված
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2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
name
The antimalarial agent mefloquine inhibits ATP-sensitive K-channels.
@en
type
label
The antimalarial agent mefloquine inhibits ATP-sensitive K-channels.
@en
prefLabel
The antimalarial agent mefloquine inhibits ATP-sensitive K-channels.
@en
P2093
P2860
P356
P1476
The antimalarial agent mefloquine inhibits ATP-sensitive K-channels.
@en
P2093
C E Higham
F M Ashcroft
F M Gribble
P2860
P304
P356
10.1038/SJ.BJP.0703638
P407
P577
2000-10-01T00:00:00Z