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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):
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.