Amin AS, Asghari-Roodsari A, Tan HL. (2010). Cardiac sodium channelopathies. Pflugers Archiv : European journal of physiology. 460 [PubMed]
An RH, Bangalore R, Rosero SZ, Kass RS. (1996). Lidocaine block of LQT-3 mutant human Na+ channels. Circulation research. 79 [PubMed]
Balser JR et al. (1996). Local anesthetics as effectors of allosteric gating. Lidocaine effects on inactivation-deficient rat skeletal muscle Na channels. The Journal of clinical investigation. 98 [PubMed]
Balser JR, Nuss HB, Romashko DN, Marban E, Tomaselli GF. (1996). Functional consequences of lidocaine binding to slow-inactivated sodium channels. The Journal of general physiology. 107 [PubMed]
Bankston JR et al. (2007). A novel and lethal de novo LQT-3 mutation in a newborn with distinct molecular pharmacology and therapeutic response. PloS one. 2 [PubMed]
Bennett PB, Valenzuela C, Chen LQ, Kallen RG. (1995). On the molecular nature of the lidocaine receptor of cardiac Na+ channels. Modification of block by alterations in the alpha-subunit III-IV interdomain. Circulation research. 77 [PubMed]
Bennett PB, Yazawa K, Makita N, George AL. (1995). Molecular mechanism for an inherited cardiac arrhythmia. Nature. 376 [PubMed]
Butterworth JF, Strichartz GR. (1990). Molecular mechanisms of local anesthesia: a review. Anesthesiology. 72 [PubMed]
Chen Q et al. (1998). Genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature. 392 [PubMed]
Clancy CE, Tateyama M, Kass RS. (2002). Insights into the molecular mechanisms of bradycardia-triggered arrhythmias in long QT-3 syndrome. The Journal of clinical investigation. 110 [PubMed]
Courtemanche M, Ramirez RJ, Nattel S. (1998). Ionic mechanisms underlying human atrial action potential properties: insights from a mathematical model. The American journal of physiology. 275 [PubMed]
Craelius W, Green WL, Harris DR. (1990). Acute effects of thyroid hormone on sodium currents in neonatal myocytes. Bioscience reports. 10 [PubMed]
Dumaine R, Kirsch GE. (1998). Mechanism of lidocaine block of late current in long Q-T mutant Na+ channels. The American journal of physiology. 274 [PubMed]
Gaughan JP, Hefner CA, Houser SR. (1998). Electrophysiological properties of neonatal rat ventricular myocytes with alpha1-adrenergic-induced hypertrophy. The American journal of physiology. 275 [PubMed]
Gellens ME et al. (1992). Primary structure and functional expression of the human cardiac tetrodotoxin-insensitive voltage-dependent sodium channel. Proceedings of the National Academy of Sciences of the United States of America. 89 [PubMed]
Grant AO, Chandra R, Keller C, Carboni M, Starmer CF. (2000). Block of wild-type and inactivation-deficient cardiac sodium channels IFM/QQQ stably expressed in mammalian cells. Biophysical journal. 79 [PubMed]
Hanck DA et al. (2009). Using lidocaine and benzocaine to link sodium channel molecular conformations to state-dependent antiarrhythmic drug affinity. Circulation research. 105 [PubMed]
Hedley PL et al. (2009). The genetic basis of long QT and short QT syndromes: a mutation update. Human mutation. 30 [PubMed]
Hille B. (1977). Local anesthetics: hydrophilic and hydrophobic pathways for the drug-receptor reaction. The Journal of general physiology. 69 [PubMed]
Hines ML, Carnevale NT. (1997). The NEURON simulation environment. Neural computation. 9 [PubMed]
Jarecki BW, Piekarz AD, Jackson JO, Cummins TR. (2010). Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents. The Journal of clinical investigation. 120 [PubMed]
Jarecki BW, Sheets PL, Jackson JO, Cummins TR. (2008). Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation. The Journal of physiology. 586 [PubMed]
Kass RS. (2006). Sodium channel inactivation in heart: a novel role of the carboxy-terminal domain. Journal of cardiovascular electrophysiology. 17 Suppl 1 [PubMed]
Kiyosue T, Arita M. (1989). Late sodium current and its contribution to action potential configuration in guinea pig ventricular myocytes. Circulation research. 64 [PubMed]
Leffler A, Herzog RI, Dib-Hajj SD, Waxman SG, Cummins TR. (2005). Pharmacological properties of neuronal TTX-resistant sodium channels and the role of a critical serine pore residue. Pflugers Archiv : European journal of physiology. 451 [PubMed]
Luo CH, Rudy Y. (1994). A dynamic model of the cardiac ventricular action potential. I. Simulations of ionic currents and concentration changes. Circulation research. 74 [PubMed]
Makita N. (2009). Phenotypic overlap of cardiac sodium channelopathies: individual-specific or mutation-specific? Circulation journal : official journal of the Japanese Circulation Society. 73 [PubMed]
Makiyama T et al. (2008). A novel SCN5A gain-of-function mutation M1875T associated with familial atrial fibrillation. Journal of the American College of Cardiology. 52 [PubMed]
McNulty MM et al. (2007). Charge at the lidocaine binding site residue Phe-1759 affects permeation in human cardiac voltage-gated sodium channels. The Journal of physiology. 581 [PubMed]
Meadows LS, Chen YH, Powell AJ, Clare JJ, Ragsdale DS. (2002). Functional modulation of human brain Nav1.3 sodium channels, expressed in mammalian cells, by auxiliary beta 1, beta 2 and beta 3 subunits. Neuroscience. 114 [PubMed]
Patton DE, West JW, Catterall WA, Goldin AL. (1992). Amino acid residues required for fast Na(+)-channel inactivation: charge neutralizations and deletions in the III-IV linker. Proceedings of the National Academy of Sciences of the United States of America. 89 [PubMed]
Ragsdale DS, McPhee JC, Scheuer T, Catterall WA. (1996). Common molecular determinants of local anesthetic, antiarrhythmic, and anticonvulsant block of voltage-gated Na+ channels. Proceedings of the National Academy of Sciences of the United States of America. 93 [PubMed]
Remme CA, Wilde AA. (2008). SCN5A overlap syndromes: no end to disease complexity? Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 10 [PubMed]
Remme CA, Wilde AA, Bezzina CR. (2008). Cardiac sodium channel overlap syndromes: different faces of SCN5A mutations. Trends in cardiovascular medicine. 18 [PubMed]
Rogart RB, Cribbs LL, Muglia LK, Kephart DD, Kaiser MW. (1989). Molecular cloning of a putative tetrodotoxin-resistant rat heart Na+ channel isoform. Proceedings of the National Academy of Sciences of the United States of America. 86 [PubMed]
Ruan Y et al. (2010). Trafficking defects and gating abnormalities of a novel SCN5A mutation question gene-specific therapy in long QT syndrome type 3. Circulation research. 106 [PubMed]
Ruan Y, Liu N, Bloise R, Napolitano C, Priori SG. (2007). Gating properties of SCN5A mutations and the response to mexiletine in long-QT syndrome type 3 patients. Circulation. 116 [PubMed]
Saint DA, Ju YK, Gage PW. (1992). A persistent sodium current in rat ventricular myocytes. The Journal of physiology. 453 [PubMed]
Sheets MF, Fozzard HA, Lipkind GM, Hanck DA. (2010). Sodium channel molecular conformations and antiarrhythmic drug affinity. Trends in cardiovascular medicine. 20 [PubMed]
Sheets MF, Hanck DA. (2007). Outward stabilization of the S4 segments in domains III and IV enhances lidocaine block of sodium channels. The Journal of physiology. 582 [PubMed]
Song Y, Shryock JC, Belardinelli L. (2008). An increase of late sodium current induces delayed afterdepolarizations and sustained triggered activity in atrial myocytes. American journal of physiology. Heart and circulatory physiology. 294 [PubMed]
Stühmer W et al. (1989). Structural parts involved in activation and inactivation of the sodium channel. Nature. 339 [PubMed]
Vassilev PM, Scheuer T, Catterall WA. (1988). Identification of an intracellular peptide segment involved in sodium channel inactivation. Science (New York, N.Y.). 241 [PubMed]
Volders PG et al. (2000). Progress in the understanding of cardiac early afterdepolarizations and torsades de pointes: time to revise current concepts. Cardiovascular research. 46 [PubMed]
Wang DW et al. (2007). Cardiac sodium channel dysfunction in sudden infant death syndrome. Circulation. 115 [PubMed]
Wang DW, Yazawa K, George AL, Bennett PB. (1996). Characterization of human cardiac Na+ channel mutations in the congenital long QT syndrome. Proceedings of the National Academy of Sciences of the United States of America. 93 [PubMed]
Wang DW, Yazawa K, Makita N, George AL, Bennett PB. (1997). Pharmacological targeting of long QT mutant sodium channels. The Journal of clinical investigation. 99 [PubMed]
Wang Q et al. (1995). SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome. Cell. 80 [PubMed]
Wang SY, Mitchell J, Moczydlowski E, Wang GK. (2004). Block of inactivation-deficient Na+ channels by local anesthetics in stably transfected mammalian cells: evidence for drug binding along the activation pathway. The Journal of general physiology. 124 [PubMed]
West JW et al. (1992). A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation. Proceedings of the National Academy of Sciences of the United States of America. 89 [PubMed]
Wilde AA, Brugada R. (2011). Phenotypical manifestations of mutations in the genes encoding subunits of the cardiac sodium channel. Circulation research. 108 [PubMed]
Yamamura K et al. (2010). A novel SCN5A mutation associated with the linker between III and IV domains of Nav1.5 in a neonate with fatal long QT syndrome. International journal of cardiology. 145 [PubMed]