Sodium channel dysfunction in inherited and acquired cardiac diseases
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[1] A. Wilde,et al. Characterization of a novel SCN5A mutation associated with Brugada syndrome reveals involvement of DIIIS4-S5 linker in slow inactivation. , 2007, Cardiovascular research.
[2] H. Tan,et al. Lethal ECG changes hidden by therapeutic hypothermia , 2007, The Lancet.
[3] P. Carmeliet,et al. Overlap Syndrome of Cardiac Sodium Channel Disease in Mice Carrying the Equivalent Mutation of Human SCN5A-1795insD , 2006, Circulation.
[4] D E Roach,et al. Decrease in density of INa is in the common final pathway to heart block in murine hearts overexpressing calcineurin. , 2006, American journal of physiology. Heart and circulatory physiology.
[5] Stefan Wagner,et al. Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels. , 2006, The Journal of clinical investigation.
[6] D. Hanck,et al. An Inner Pore Residue (Asn406) in the Nav1.5 Channel Controls Slow Inactivation and Enhances Mibefradil Block to T-Type Ca2+ Channel Levels , 2006, Molecular Pharmacology.
[7] V. Torre,et al. Origin of functional diversity among tetrameric voltage‐gated channels , 2006, Proteins.
[8] P. Shockett,et al. Slow-inactivation induced conformational change in domain 2-segment 6 of cardiac Na+ channel. , 2006, Biochemical and biophysical research communications.
[9] H. Tan. Sodium Channel Variants in Heart Disease: Expanding Horizons , 2006, Journal of cardiovascular electrophysiology.
[10] J. Balser,et al. Calcium-dependent regulation of the voltage-gated sodium channel hH1: intrinsic and extrinsic sensors use a common molecular switch. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[11] T. Opthof,et al. Larger Cell Size in Rabbits With Heart Failure Increases Myocardial Conduction Velocity and QRS Duration , 2006, Circulation.
[12] Jeroen J. Bax,et al. Acceleration‐Dependent Left Bundle Branch Block with Severe Left Ventricular Dyssynchrony Results in Acute Heart Failure: Are There More Patients Who Benefit from Cardiac Resynchronization Therapy? , 2006, Journal of cardiovascular electrophysiology.
[13] A. Wilde,et al. Novel Brugada syndrome-causing mutation in ion-conducting pore of cardiac Na+ channel does not affect ion selectivity properties. , 2005, Acta physiologica Scandinavica.
[14] Simona Casini,et al. Right Ventricular Fibrosis and Conduction Delay in a Patient With Clinical Signs of Brugada Syndrome: A Combined Electrophysiological, Genetic, Histopathologic, and Computational Study , 2005, Circulation.
[15] J. D. de Bakker,et al. Impaired Impulse Propagation in Scn5a-Knockout Mice: Combined Contribution of Excitability, Connexin Expression, and Tissue Architecture in Relation to Aging , 2005, Circulation.
[16] G. Weidinger,et al. Prognostic value of the QRS duration in patients with heart failure: a subgroup analysis from 24 centers of Val-HeFT. , 2005, Journal of cardiac failure.
[17] A. Wilde,et al. Pathophysiological mechanisms of Brugada syndrome: depolarization disorder, repolarization disorder, or more? , 2005, Cardiovascular research.
[18] A. Wilde,et al. Substitution of a conserved alanine in the domain IIIS4-S5 linker of the cardiac sodium channel causes long QT syndrome. , 2005, Cardiovascular research.
[19] L L Isom,et al. Sodium channels as macromolecular complexes: implications for inherited arrhythmia syndromes. , 2005, Cardiovascular research.
[20] Magali Bouhours,et al. A1152D mutation of the Na+ channel causes paramyotonia congenita and emphasizes the role of DIII/S4–S5 linker in fast inactivation , 2005, The Journal of physiology.
[21] K. Imoto,et al. A Novel Missense Mutation in the SCN5A Gene Associated with Brugada Syndrome Bidirectionally Affecting Blocking Actions of Antiarrhythmic Drugs , 2005, Journal of cardiovascular electrophysiology.
[22] C. Valdivia,et al. Increased late sodium current in myocytes from a canine heart failure model and from failing human heart. , 2005, Journal of molecular and cellular cardiology.
[23] Y. Okumura,et al. Double SCN5A mutation underlying asymptomatic Brugada syndrome. , 2005, Heart rhythm.
[24] Shin-Ho Chung,et al. A model of sodium channels. , 2005, Biochimica et biophysica acta.
[25] Jeffrey L. Anderson,et al. Sodium channel mutations and susceptibility to heart failure and atrial fibrillation. , 2005, JAMA.
[26] Carlo Napolitano,et al. Nav1.5 E1053K mutation causing Brugada syndrome blocks binding to ankyrin-G and expression of Nav1.5 on the surface of cardiomyocytes. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[27] Walter Birchmeier,et al. Mutations in the desmosomal protein plakophilin-2 are common in arrhythmogenic right ventricular cardiomyopathy , 2004, Nature Genetics.
[28] R. Kass,et al. Calmodulin Mediates Ca2+ Sensitivity of Sodium Channels* , 2004, Journal of Biological Chemistry.
[29] S. Nattel,et al. Post-transcriptional alterations in the expression of cardiac Na+ channel subunits in chronic heart failure. , 2004, Journal of molecular and cellular cardiology.
[30] S. Peters,et al. Results of ajmaline testing in patients with arrhythmogenic right ventricular dysplasia-cardiomyopathy. , 2004, International journal of cardiology.
[31] W. Haverkamp,et al. Images in cardiovascular medicine. Life-threatening neonatal arrhythmia: successful treatment and confirmation of clinically suspected extreme long QT-syndrome-3. , 2004, Circulation.
[32] A. Wilde,et al. Delay in Right Ventricular Activation Contributes to Brugada Syndrome , 2004, Circulation.
[33] T. Lybrand,et al. An EF-hand in the sodium channel couples intracellular calcium to cardiac excitability , 2004, Nature Structural &Molecular Biology.
[34] A. van Oosterom,et al. ECGSIM: an interactive tool for studying the genesis of QRST waveforms , 2004, Heart.
[35] G. Breithardt,et al. Long QT syndrome and life threatening arrhythmia in a newborn: molecular diagnosis and treatment response , 2003, Heart.
[36] A. Iwasa,et al. Mechanism of ST Elevation and Ventricular Arrhythmias in an Experimental Brugada Syndrome Model , 2003, Circulation.
[37] Ruben Coronel,et al. Intrinsic heterogeneity in repolarization is increased in isolated failing rabbit cardiomyocytes during simulated ischemia. , 2003, Cardiovascular research.
[38] H. Tan,et al. Genetic control of sodium channel function. , 2003, Cardiovascular research.
[39] H. Jongsma,et al. A novel LQT3 mutation implicates the human cardiac sodium channel domain IVS6 in inactivation kinetics. , 2003, Cardiovascular research.
[40] R. Coronel,et al. [Na+]i and the driving force of the Na+/Ca2+-exchanger in heart failure. , 2003, Cardiovascular research.
[41] Lucas J Herfst,et al. Compound Heterozygosity for Mutations (W156X and R225W) in SCN5A Associated With Severe Cardiac Conduction Disturbances and Degenerative Changes in the Conduction System , 2003, Circulation research.
[42] P. C. Viswanathan,et al. A common SCN5A polymorphism modulates the biophysical effects of an SCN5A mutation. , 2003, The Journal of clinical investigation.
[43] J. Brugada,et al. Brugada syndrome: a decade of progress. , 2002, Circulation research.
[44] R. Hauer,et al. Proposed diagnostic criteria for the Brugada syndrome: consensus report. , 2002, Circulation.
[45] G. Danieli,et al. Mutation in human desmoplakin domain binding to plakoglobin causes a dominant form of arrhythmogenic right ventricular cardiomyopathy. , 2002, American journal of human genetics.
[46] Cornelis A. Grimbergen,et al. Software design for analysis of multichannel intracardial and body surface electrocardiograms , 2002, Comput. Methods Programs Biomed..
[47] H. N. Sabbah,et al. Down-regulation of sodium current in chronic heart failure: effect of long-term therapy with carvedilol , 2002, Cellular and Molecular Life Sciences CMLS.
[48] P. Brugada,et al. Heart Transplantation as Last Resort Against Brugada Syndrome , 2002, Journal of cardiovascular electrophysiology.
[49] G. Breithardt,et al. Genotype-phenotype relationship in Brugada syndrome: electrocardiographic features differentiate SCN5A-related patients from non-SCN5A-related patients. , 2002, Journal of the American College of Cardiology.
[50] H. Morita,et al. Epicardial electrogram of the right ventricular outflow tract in patients with the Brugada syndrome: using the epicardial lead. , 2002, Journal of the American College of Cardiology.
[51] S. Fisher,et al. QRS duration and mortality in patients with congestive heart failure. , 2002, American heart journal.
[52] U. Gerckens,et al. [Brugada syndrome or ARVD (arrhythmogenic right ventricular dysplasia) or both? Significance and value of right precordial ECG changes]. , 2002, Zeitschrift fur Kardiologie.
[53] N. Makita,et al. A mutant cardiac sodium channel with multiple biophysical defects associated with overlapping clinical features of Brugada syndrome and cardiac conduction disease. , 2002, Cardiovascular research.
[54] Mark E. Anderson,et al. A calcium sensor in the sodium channel modulates cardiac excitability , 2002, Nature.
[55] P. C. Viswanathan,et al. Clinical, Genetic, and Biophysical Characterization of SCN5A Mutations Associated With Atrioventricular Conduction Block , 2002, Circulation.
[56] Ruben Coronel,et al. Activation Delay After Premature Stimulation in Chronically Diseased Human Myocardium Relates to the Architecture of Interstitial Fibrosis , 2001, Circulation.
[57] Y. Hirano,et al. Identical unitary current amplitude and Ca(2+) block of cardiac Na channel before and during beta-adrenergic stimulation. , 2001, The Japanese journal of physiology.
[58] Bortolo Martini,et al. Brugada by any other name? , 2001, European heart journal.
[59] G. Breithardt,et al. De Novo Mutation in the SCN5A Gene Associated With Early Onset of Sudden Infant Death , 2001, Circulation.
[60] T. Nakagawa,et al. Solution structures of the cytoplasmic linkers between segments S4 and S5 (S4-S5) in domains III and IV of human brain sodium channels in SDS micelles. , 2001, The journal of peptide research : official journal of the American Peptide Society.
[61] S. Priori,et al. Inherited Brugada and Long QT-3 Syndrome Mutations of a Single Residue of the Cardiac Sodium Channel Confer Distinct Channel and Clinical Phenotypes* , 2001, The Journal of Biological Chemistry.
[62] K. Murray,et al. Conventional protein kinase C isoforms and cross‐activation of protein kinase A regulate cardiac Na+ current , 2001, FEBS letters.
[63] J. Balser,et al. The cardiac sodium channel: gating function and molecular pharmacology. , 2001, Journal of molecular and cellular cardiology.
[64] P. C. Viswanathan,et al. A sodium-channel mutation causes isolated cardiac conduction disease , 2001, Nature.
[65] D. Corrado,et al. Right Bundle Branch Block, Right Precordial ST-Segment Elevation, and Sudden Death in Young People , 2001, Circulation.
[66] D. Stephan,et al. Identification of mutations in the cardiac ryanodine receptor gene in families affected with arrhythmogenic right ventricular cardiomyopathy type 2 (ARVD2). , 2001, Human molecular genetics.
[67] J. Balser,et al. Enhanced Na(+) channel intermediate inactivation in Brugada syndrome. , 2000, Circulation research.
[68] R. Coronel,et al. Laplacian Electrograms and the Interpretation of Complex Ventricular Activation Patterns During Ventricular Fibrillation , 2000, Journal of cardiovascular electrophysiology.
[69] P. C. Viswanathan,et al. Two distinct congenital arrhythmias evoked by a multidysfunctional Na(+) channel. , 2000, Circulation research.
[70] A. Wilde,et al. A single Na(+) channel mutation causing both long-QT and Brugada syndromes. , 1999, Circulation research.
[71] J. Towbin,et al. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. , 1999, Circulation research.
[72] C. Antzelevitch,et al. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. , 1999, Circulation.
[73] D. Maclennan,et al. HEK-293 cells possess a carbachol- and thapsigargin-sensitive intracellular Ca2+ store that is responsive to stop-flow medium changes and insensitive to caffeine and ryanodine , 1999 .
[74] R. Winslow,et al. Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, II: model studies. , 1999, Circulation research.
[75] R. Meyer,et al. Control of L‐type calcium current during the action potential of guinea‐pig ventricular myocytes , 1998, The Journal of physiology.
[76] N. Chehab,et al. Glutamine Substitution at Alanine1649 in the S4–S5 Cytoplasmic Loop of Domain 4 Removes the Voltage Sensitivity of Fast Inactivation in the Human Heart Sodium Channel , 1998, The Journal of general physiology.
[77] R. Virmani,et al. Arrhythmogenic right ventricular cardiomyopathy and fatty replacement of the right ventricular myocardium: are they different diseases? , 1998, Circulation.
[78] J. Thompson,et al. The CLUSTAL_X windows interface: flexible strategies for multiple sequence alignment aided by quality analysis tools. , 1997, Nucleic acids research.
[79] H Kasanuki,et al. Idiopathic ventricular fibrillation induced with vagal activity in patients without obvious heart disease. , 1997, Circulation.
[80] K. Murray,et al. Functional effects of protein kinase C activation on the human cardiac Na+ channel. , 1997, Circulation research.
[81] P. Ruben,et al. Interaction between fast and slow inactivation in Skm1 sodium channels. , 1996, Biophysical journal.
[82] A. George,et al. Characterization of human cardiac Na+ channel mutations in the congenital long QT syndrome. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[83] P. Schwartz,et al. Multiple mechanisms of Na+ channel--linked long-QT syndrome. , 1996, Circulation research.
[84] D. Corrado,et al. Familial cardiomyopathy underlies syndrome of right bundle branch block, ST segment elevation and sudden death. , 1996, Journal of the American College of Cardiology.
[85] D. Kass,et al. Ionic mechanism of action potential prolongation in ventricular myocytes from dogs with pacing-induced heart failure. , 1996, Circulation research.
[86] R. French,et al. Sodium current inhibition by internal calcium: A combination of open-channel block and surface charge screening? , 1995, The Journal of Membrane Biology.
[87] A. George,et al. Molecular mechanism for an inherited cardiac arrhythmia , 1995, Nature.
[88] H. Duff,et al. Effects of intracellular calcium on sodium current density in cultured neonatal rat cardiac myocytes. , 1995, The Journal of physiology.
[89] J M de Bakker,et al. Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts. , 1994, Cardiovascular research.
[90] W. Catterall,et al. Modulation of cardiac Na+ channels expressed in a mammalian cell line and in ventricular myocytes by protein kinase C. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[91] W. Wonderlin,et al. Ion Permeation, Divalent Ion Block, and Chemical Modification of Single Sodium Channels Description by Single- and Double-occupancy Rate-Theory Models , 1994 .
[92] H. Matsuda,et al. Voltage‐dependent block by internal Ca2+ ions of inwardly rectifying K+ channels in guinea‐pig ventricular cells. , 1993, The Journal of physiology.
[93] Z. Fan,et al. Properties of veratridine-modified single Na+ channels in guinea pig ventricular myocytes , 1993 .
[94] A L Goldin,et al. A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[95] T. Opthof,et al. Reperfusion arrhythmias in isolated perfused pig hearts. Inhomogeneities in extracellular potassium, ST and TQ potentials, and transmembrane action potentials. , 1992, Circulation research.
[96] W. Catterall,et al. Class I and IV antiarrhythmic drugs and cytosolic calcium regulate mRNA encoding the sodium channel alpha subunit in rat cardiac muscle. , 1992, Molecular pharmacology.
[97] R. C. Saumarez,et al. Ventricular Fibrillation in Hypertrophic Cardiomyopathy Is Associated With Increased Fractionation of Paced Right Ventricular Electrograms , 1992, Circulation.
[98] N. Tohse,et al. Calcium-sensitive delayed rectifier potassium current in guinea pig ventricular cells. , 1990, The American journal of physiology.
[99] L. Hondeghem,et al. Stretch-induced arrhythmias in the isolated canine ventricle. Evidence for the importance of mechanoelectrical feedback. , 1990, Circulation.
[100] H A Fozzard,et al. Nonlinear Relation Between ±max and INa in Canine Cardiac Purkinje Cells , 1988, Circulation research.
[101] B. Nilius. Calcium block of guinea‐pig heart sodium channels with and without modification by the piperazinylindole DPI 201‐106. , 1988, The Journal of physiology.
[102] V. Froelicher,et al. Normal Electrocardiographic Waveform Characteristics During Treadmill Exercise Testing , 1979, Circulation.
[103] R. Eckert,et al. Calcium entry leads to inactivation of calcium channel in Paramecium. , 1978, Science.
[104] M. Simoons,et al. Gradual Changes of ECG Waveform During and After Exercise in Normal Subjects , 1975, Circulation.
[105] Joseph Tranquillo,et al. Sodium channel kinetic changes that produce Brugada syndrome or progressive cardiac conduction system disease. , 2007, American journal of physiology. Heart and circulatory physiology.
[106] D. Bers,et al. Cardiac myocytes Ca2+ and Na+ regulation in normal and failing hearts. , 2006, Journal of pharmacological sciences.
[107] D. Roden,et al. Cloning and initial characterization of the human cardiac sodium channel (SCN5A) promoter. , 2004, Cardiovascular research.
[108] Bortolo Martini,et al. 1988-2003. Fifteen years after the first Italian description by Nava-Martini-Thiene and colleagues of a new syndrome (different from the Brugada syndrome?) in the Giornale Italiano di Cardiologia: do we really know everything on this entity? , 2004, Italian heart journal : official journal of the Italian Federation of Cardiology.
[109] G. Steinbeck,et al. Regional differences in current density and rate-dependent properties of the transient outward current in subepicardial and subendocardial myocytes of human left ventricle. , 1996, Circulation.
[110] R. Lux,et al. Correlation between in vivo transmembrane action potential durations and activation-recovery intervals from electrograms. Effects of interventions that alter repolarization time. , 1990, Circulation.
[111] G. Moe. Oscillating concepts in arrhythmia research; a personal account. , 1984, International journal of cardiology.