Papers associated with heart (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;
	Differential regulation of cardiac sodium channels by intracellular fibroblast growth factors., Angsutararux P., J Gen Physiol. May 1, 2023; 155 (5):
	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.
	Splicing misregulation of SCN5A contributes to cardiac-conduction delay and heart arrhythmia in myotonic dystrophy., Freyermuth F., Nat Commun. April 11, 2016; 7 11067.
	Voltage-dependent blockade by bupivacaine of cardiac sodium channels expressed in Xenopus oocytes., Zhang H., Neurosci Bull. August 1, 2014; 30 (4): 697-710.
	Gain-of-function mutation in TASK-4 channels and severe cardiac conduction disorder., Friedrich C., EMBO Mol Med. July 1, 2014; 6 (7): 937-51.
	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.
	Pharmacological modulation of brain Nav1.2 and cardiac Nav1.5 subtypes by the local anesthetic ropivacaine., Cheng HW., Neurosci Bull. August 1, 2010; 26 (4): 289-96.
	Blocking effect of methylflavonolamine on human Na(V)1.5 channels expressed in Xenopus laevis oocytes and on sodium currents in rabbit ventricular myocytes., Fan XR., Acta Pharmacol Sin. March 1, 2010; 31 (3): 297-306.
	Correlations between clinical and physiological consequences of the novel mutation R878C in a highly conserved pore residue in the cardiac Na+ channel., Zhang Y., Acta Physiol (Oxf). December 1, 2008; 194 (4): 311-23.
	Nav channel mechanosensitivity: activation and inactivation accelerate reversibly with stretch., Morris CE., Biophys J. August 1, 2007; 93 (3): 822-33.
	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.
	GLUT8 is dispensable for embryonic development but influences hippocampal neurogenesis and heart function., Membrez M., Mol Cell Biol. June 1, 2006; 26 (11): 4268-76.
	Distribution and functional characterization of human Nav1.3 splice variants., Thimmapaya R., Eur J Neurosci. July 1, 2005; 22 (1): 1-9.
	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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