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Extracellular cysteine disulfide bond break at Cys122 disrupts PIP 2 -dependent Kir2.1 channel function and leads to arrhythmias in Andersen-Tawil Syndrome. , Cruz FM., bioRxiv. June 8, 2023;
The G213D variant in Nav1.5 alters sodium current and causes an arrhythmogenic phenotype resulting in a multifocal ectopic Purkinje-related premature contraction phenotype in human-induced pluripotent stem cell-derived cardiomyocytes. , Calloe K., Europace. December 9, 2022; 24 (12): 2015-2027.
Identification of SCN5a p.C335R Variant in a Large Family with Dilated Cardiomyopathy and Conduction Disease. , Sedaghat-Hamedani F., Int J Mol Sci. November 30, 2021; 22 (23):
Polyunsaturated fatty acid analogues differentially affect cardiac NaV, CaV, and KV channels through unique mechanisms. , Bohannon BM., Elife. March 24, 2020; 9
Molecular charge associated with antiarrhythmic actions in a series of amino-2-cyclohexyl ester derivatives. , Pugsley MK., Eur J Pharmacol. February 5, 2019; 844 241-252.
Voltage-dependent blockade by bupivacaine of cardiac sodium channels expressed in Xenopus oocytes. , Zhang H ., Neurosci Bull. August 1, 2014; 30 (4): 697-710.
A proton leak current through the cardiac sodium channel is linked to mixed arrhythmia and the dilated cardiomyopathy phenotype. , Gosselin-Badaroudine P., PLoS One. January 1, 2012; 7 (5): e38331.
Solution structure of Jingzhaotoxin-III, a peptide toxin inhibiting both Nav1.5 and Kv2.1 channels. , Liao Z., Toxicon. July 1, 2007; 50 (1): 135-43.
Occurrence of a tetrodotoxin-sensitive calcium current in rat ventricular myocytes after long-term myocardial infarction. , Alvarez JL., Cardiovasc Res. September 1, 2004; 63 (4): 653-61.
Inhibition of cardiac sodium currents by toluene exposure. , Cruz SL., Br J Pharmacol. October 1, 2003; 140 (4): 653-60.