Papers associated with cardiac myocyte (and nav1)

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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
	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.

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