Papers associated with heart (and scn5a)

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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):
	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.
	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.
	Identification and characterisation of a novel KCNQ1 mutation in a family with Romano-Ward syndrome., Zehelein J., Biochim Biophys Acta. November 5, 2004; 1690 (3): 185-92.
	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.
	Compound heterozygosity for mutations (W156X and R225W) in SCN5A associated with severe cardiac conduction disturbances and degenerative changes in the conduction system., Bezzina CR., Circ Res. February 7, 2003; 92 (2): 159-68.
	Cocaine binds to a common site on open and inactivated human heart (Na(v)1.5) sodium channels., O'Leary ME., J Physiol. June 15, 2002; 541 (Pt 3): 701-16.
	The sodium channel beta-subunit SCN3b modulates the kinetics of SCN5a and is expressed heterogeneously in sheep heart., Fahmi AI., J Physiol. December 15, 2001; 537 (Pt 3): 693-700.
	Novel mechanism for Brugada syndrome: defective surface localization of an SCN5A mutant (R1432G)., Baroudi G., Circ Res. June 22, 2001; 88 (12): E78-83.
	Functional suppression of sodium channels by beta(1)-subunits as a molecular mechanism of idiopathic ventricular fibrillation., Wan X., J Mol Cell Cardiol. October 1, 2000; 32 (10): 1873-84.
	Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome., Rook MB., Cardiovasc Res. December 1, 1999; 44 (3): 507-17.
	Molecular mechanism for an inherited cardiac arrhythmia., Bennett PB., Nature. August 24, 1995; 376 (6542): 683-5.

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