The cardiac sodium channel: gating function and molecular pharmacology.
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[1] Francisco Bezanilla,et al. Voltage Sensors in Domains III and IV, but Not I and II, Are Immobilized by Na+ Channel Fast Inactivation , 1999, Neuron.
[2] R. Kass,et al. Lidocaine block of LQT-3 mutant human Na+ channels. , 1996, Circulation research.
[3] C. Antzelevitch,et al. Differences in the Electrophysiological Response of Canine Ventricular Epicardium and Endocardium to Ischemia Role of the Transient Outward Current , 1993, Circulation.
[4] L. Kiss,et al. Contribution of the selectivity filter to inactivation in potassium channels. , 1999, Biophysical journal.
[5] R. Horn,et al. Evidence for voltage-dependent S4 movement in sodium channels , 1995, Neuron.
[6] P. C. Viswanathan,et al. Two distinct congenital arrhythmias evoked by a multidysfunctional Na(+) channel. , 2000, Circulation research.
[7] B. Katzung,et al. Time- and voltage-dependent interactions of antiarrhythmic drugs with cardiac sodium channels. , 1977, Biochimica et biophysica acta.
[8] H. Lerche,et al. Role in fast inactivation of the IV/S4–S5 loop of the human muscle Na+ channel probed by cysteine mutagenesis , 1997, The Journal of physiology.
[9] C. Antzelevitch,et al. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. , 1999, Circulation.
[10] D M Roden,et al. Congenital long-QT syndrome caused by a novel mutation in a conserved acidic domain of the cardiac Na+ channel. , 1999, Circulation.
[11] P. Ruben,et al. Structural determinants of slow inactivation in human cardiac and skeletal muscle sodium channels. , 1999, Biophysical journal.
[12] B. Hille,et al. Local anesthetics: hydrophilic and hydrophobic pathways for the drug- receptor reaction , 1977, The Journal of general physiology.
[13] Priya D. Duggal,et al. Sodium channel abnormalities are infrequent in patients with long QT syndrome: identification of two novel SCN5A mutations. , 1999, American journal of medical genetics.
[14] H. Takeshima,et al. Expression of functional sodium channels from cloned cDNA , 1986, Nature.
[15] B. Kerem,et al. Molecular pharmacology of the sodium channel mutation D1790G linked to the long-QT syndrome. , 2000, Circulation.
[16] H. Fozzard,et al. Structure and function of voltage-dependent sodium channels: comparison of brain II and cardiac isoforms. , 1996, Physiological reviews.
[17] Eduardo Marbán,et al. Lidocaine induces a slow inactivated state in rat skeletal muscle sodium channels , 2000, The Journal of physiology.
[18] A. Hodgkin,et al. A quantitative description of membrane current and its application to conduction and excitation in nerve , 1952, The Journal of physiology.
[19] M. Cahalan. Local anesthetic block of sodium channels in normal and pronase-treated squid giant axons. , 1978, Biophysical journal.
[20] C Antzelevitch,et al. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. , 1999, Circulation research.
[21] G. Tomaselli,et al. Structure and function of voltage‐gated sodium channels , 1998, The Journal of physiology.
[22] G. Yellen,et al. Dynamic Rearrangement of the Outer Mouth of a K+ Channel during Gating , 1996, Neuron.
[23] G. Ndrepepa,et al. Actions of lidocaine on reentrant ventricular rhythms in the subacute myocardial infarction period in dogs. , 1997, The American journal of physiology.
[24] D. Ragsdale,et al. A molecular basis for the different local anesthetic affinities of resting versus open and inactivated states of the sodium channel. , 1999, Molecular pharmacology.
[25] M. Chahine,et al. SCN5A mutation (T1620M) causing Brugada syndrome exhibits different phenotypes when expressed in Xenopus oocytes and mammalian cells , 2000, FEBS letters.
[26] W. Catterall,et al. From Ionic Currents to Molecular Mechanisms The Structure and Function of Voltage-Gated Sodium Channels , 2000, Neuron.
[27] J. Balser. Structure and function of the cardiac sodium channels. , 1999, Cardiovascular research.
[28] J. Pu,et al. Alterations of Na+ currents in myocytes from epicardial border zone of the infarcted heart. A possible ionic mechanism for reduced excitability and postrepolarization refractoriness. , 1997, Circulation research.
[29] R. Myerburg,et al. Electrophysiological properties and responses to simulated ischemia in cat ventricular myocytes of endocardial and epicardial origin. , 1990, Circulation research.
[30] J. Balser,et al. Mechanistic link between lidocaine block and inactivation probed by outer pore mutations in the rat μ1 skeletal muscle sodium channel , 1998, The Journal of physiology.
[31] A. Wilde,et al. A single Na(+) channel mutation causing both long-QT and Brugada syndromes. , 1999, Circulation research.
[32] R. Horn,et al. Role of an S4-S5 linker in sodium channel inactivation probed by mutagenesis and a peptide blocker , 1996, The Journal of general physiology.
[33] G. Breithardt,et al. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation , 1998, Nature.
[34] K. Gingrich,et al. Ultra‐deep blockade of Na+ channels by a quaternary ammonium ion: catalysis by a transition‐intermediate state? , 1993, The Journal of physiology.
[35] R Horn,et al. Primary structure and functional expression of the human cardiac tetrodotoxin-insensitive voltage-dependent sodium channel. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[36] Slow inactivation of sodium channels: more than just a laboratory curiosity. , 1996, Biophysical journal.
[37] R. Horn,et al. Independent Versus Coupled Inactivation in Sodium Channels , 1998, The Journal of general physiology.
[38] J. Balser,et al. A revised view of cardiac sodium channel "blockade" in the long-QT syndrome. , 2000, The Journal of clinical investigation.
[39] J Benhorin,et al. Arrhythmogenic mechanism of an LQT-3 mutation of the human heart Na(+) channel alpha-subunit: A computational analysis. , 2000, Circulation.
[40] Kinetic effects of quaternary lidocaine block of cardiac sodium channels: a gating current study , 1994, The Journal of general physiology.
[41] F Bezanilla,et al. Inactivation of the sodium channel. II. Gating current experiments , 1977, The Journal of general physiology.
[42] W. Catterall,et al. Inhibition of inactivation of single sodium channels by a site-directed antibody. , 1989, Proceedings of the National Academy of Sciences of the United States of America.
[43] Ming Zhou,et al. Sodium channel mutations in paramyotonia congenita uncouple inactivation from activation , 1994, Neuron.
[44] J. Balser,et al. Local anesthetics as effectors of allosteric gating. Lidocaine effects on inactivation-deficient rat skeletal muscle Na channels. , 1996, The Journal of clinical investigation.
[45] G. Tomaselli,et al. Molecular motions within the pore of voltage-dependent sodium channels. , 1997, Biophysical journal.
[46] B. Chait,et al. The structure of the potassium channel: molecular basis of K+ conduction and selectivity. , 1998, Science.
[47] J. Balser. Sodium "channelopathies" and sudden death: must you be so sensitive? , 1999, Circulation research.
[48] L. Vyklický,et al. Changes of of extracellular potassium concentration induced by neuronal activity in the spinal cord of the cat , 1974, The Journal of physiology.
[49] B. Sakmann,et al. Molecular basis of functional diversity of voltage‐gated potassium channels in mammalian brain. , 1989, The EMBO journal.
[50] E. Isacoff,et al. Molecular Coupling of S4 to a K+ Channel's Slow Inactivation Gate , 2000, The Journal of general physiology.
[51] B. Khodorov,et al. Ca-sensitive slow inactivation and lidocaine-induced block of sodium channels in rat cardiac cells. , 1991, Journal of molecular and cellular cardiology.
[52] W. Catterall,et al. Common molecular determinants of local anesthetic, antiarrhythmic, and anticonvulsant block of voltage-gated Na+ channels. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[53] G. Tomaselli,et al. Ion channels as enzymes: analogy or homology? , 1997, Trends in Neurosciences.
[54] R. Matsuoka,et al. A de novo missense mutation of human cardiac Na+ channel exhibiting novel molecular mechanisms of long QT syndrome , 1998, FEBS letters.
[55] F. Conti,et al. Structural parts involved in activation and inactivation of the sodium channel , 1989, Nature.
[56] B. Kerem,et al. Novel LQT-3 Mutation Affects Na+ Channel Activity Through Interactions Between α- and β1-Subunits , 1998 .
[57] P. Backx,et al. P-loop Flexibility in Na+ Channel Pores Revealed by Single- and Double-cysteine Replacements , 1997, The Journal of general physiology.
[58] J. Brugada,et al. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. , 1992, Journal of the American College of Cardiology.
[59] J. Balser,et al. External pore residue mediates slow inactivation in mu 1 rat skeletal muscle sodium channels. , 1996, The Journal of physiology.
[60] C. Antzelevitch,et al. Sodium channel block produces opposite electrophysiological effects in canine ventricular epicardium and endocardium. , 1991, Circulation research.
[61] C. Armstrong,et al. Fast and slow steps in the activation of sodium channels , 1979, The Journal of general physiology.
[62] W. Stühmer,et al. Calcium channel characteristics conferred on the sodium channel by single mutations , 1992, Nature.
[63] H. Fozzard,et al. Ultra-slow inactivation in mu1 Na+ channels is produced by a structural rearrangement of the outer vestibule. , 1999, Biophysical journal.
[64] J. Balser,et al. Functional consequences of lidocaine binding to slow-inactivated sodium channels , 1996, The Journal of general physiology.
[65] 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.
[66] S. Y. Wang,et al. Local anesthetic block of batrachotoxin-resistant muscle Na+ channels. , 1998, Molecular pharmacology.
[67] 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.
[68] Arthur J Moss,et al. SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome , 1995, Cell.
[69] J. Trimmer,et al. Primary structure and functional expression of a mammalian skeletal muscle sodium channel , 1989, Neuron.
[70] A. L. Goldin,et al. Interaction between the sodium channel inactivation linker and domain III S4-S5. , 1997, Biophysical journal.
[71] J. Balser,et al. Molecular Dynamics of the Sodium Channel Pore Vary with Gating: Interactions between P-Segment Motions and Inactivation , 1999, The Journal of Neuroscience.
[72] G. Ndrepepa,et al. Reentrant arrhythmias in the subacute infarction period. The proarrhythmic effect of flecainide acetate on functional reentrant circuits. , 1995, Circulation.
[73] Robert L. Barchi,et al. Inactivation and Secondary Structure in the D4/S4-5 Region of the SkM1 Sodium Channel , 1998, The Journal of general physiology.
[74] A. George,et al. Pharmacological targeting of long QT mutant sodium channels. , 1997, The Journal of clinical investigation.
[75] W. Catterall,et al. A Critical Role for the S4-S5 Intracellular Loop in Domain IV of the Sodium Channel α-Subunit in Fast Inactivation* , 1998, The Journal of Biological Chemistry.
[76] N. Makita,et al. Enhanced sodium channel intermediate inactivation in Brugada syndrome , 2000 .
[77] A. Wilde,et al. "Brugada" syndrome: clinical data and suggested pathophysiological mechanism. , 1999, Circulation.
[78] G. Strichartz,et al. Point mutations at N434 in D1-S6 of mu1 Na(+) channels modulate binding affinity and stereoselectivity of local anesthetic enantiomers. , 1999, Molecular pharmacology.
[79] B. Kerem,et al. Novel LQT-3 mutation affects Na+ channel activity through interactions between alpha- and beta1-subunits. , 1998, Circulation research.
[80] J. Balser,et al. Isoform-specific lidocaine block of sodium channels explained by differences in gating. , 2000, Biophysical journal.
[81] J. Balser,et al. Lidocaine action on Na+ currents in ventricular myocytes from the epicardial border zone of the infarcted heart. , 1998, Circulation research.
[82] J. Yeh. Sodium inactivation mechanism modulates QX-314 block of sodium channels in squid axons. , 1978, Biophysical journal.
[83] J. Makielski,et al. Slowly Recovering Cardiac Sodium Current in Rat Ventricular Myocytes: Effects of Conditioning Duration and Recovery Potential , 1995, Journal of cardiovascular electrophysiology.
[84] B. Rudy,et al. Slow inactivation of the sodium conductance in squid giant axons. Pronase resistance. , 1978, The Journal of physiology.
[85] P. Bennett,et al. On the molecular nature of the lidocaine receptor of cardiac Na+ channels. Modification of block by alterations in the alpha-subunit III-IV interdomain. , 1995, Circulation research.
[86] K. Courtney. Mechanism of frequency-dependent inhibition of sodium currents in frog myelinated nerve by the lidocaine derivative GEA. , 1975, The Journal of pharmacology and experimental therapeutics.
[87] C. Stevens,et al. Sodium channels need not open before they inactivate , 1981, Nature.
[88] R. Horn,et al. Role of Domain 4 in Sodium Channel Slow Inactivation , 2000, The Journal of general physiology.
[89] W. Catterall,et al. A Critical Role for Transmembrane Segment IVS6 of the Sodium Channel α Subunit in Fast Inactivation (*) , 1995, The Journal of Biological Chemistry.
[90] Y. Aizawa,et al. Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome. , 1996, Journal of the American College of Cardiology.
[91] C. Antzelevitch,et al. Flecainide‐Induced Arrhythmia in Canine Ventricular Epicardium Phase 2 Reentry? , 1993, Circulation.
[92] C. F. Stevens,et al. A reinterpretation of mammalian sodium channel gating based on single channel recording , 1983, Nature.
[93] C. Rohl,et al. Solution structure of the sodium channel inactivation gate. , 1999, Biochemistry.
[94] W. Catterall,et al. Movement of the Na+ Channel Inactivation Gate during Inactivation* , 1996, The Journal of Biological Chemistry.
[95] S. Priori,et al. The Elusive Link Between LQT3 and Brugada Syndrome: The Role of Flecainide Challenge , 2000, Circulation.
[96] I. V. Van Gelder,et al. Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome. , 1999, Cardiovascular research.
[97] H L Greene,et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. , 1991, The New England journal of medicine.
[98] P. Schwartz,et al. Multiple mechanisms of Na+ channel--linked long-QT syndrome. , 1996, Circulation research.
[99] H. Inoue,et al. ST Segment Elevation in the Right Precordial Leads Induced with Class IC Antiarrhythmic Drugs , 1999, Journal of cardiovascular electrophysiology.
[100] H. Fozzard,et al. Sodium channel selectivity filter regulates antiarrhythmic drug binding. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[101] J. Balser,et al. Phenotypic characterization of a novel long-QT syndrome mutation (R1623Q) in the cardiac sodium channel. , 1998, Circulation.
[102] A. George,et al. Molecular mechanism for an inherited cardiac arrhythmia , 1995, Nature.
[103] F. Sigworth,et al. Impaired slow inactivation in mutant sodium channels. , 1996, Biophysical journal.
[104] P. Guicheney,et al. Electrophysiological characterization of SCN5A mutations causing long QT (E1784K) and Brugada (R1512W and R1432G) syndromes. , 2000, Cardiovascular research.
[105] G. Strichartz,et al. The Inhibition of Sodium Currents in Myelinated Nerve by Quaternary Derivatives of Lidocaine , 1973, The Journal of general physiology.
[106] C F Starmer,et al. Mechanisms of use-dependent block of sodium channels in excitable membranes by local anesthetics. , 1984, Biophysical journal.
[107] A. L. Goldin,et al. Sodium Channel Activation Gating Is Affected by Substitutions of Voltage Sensor Positive Charges in All Four Domains , 1997, The Journal of general physiology.
[108] W. Catterall,et al. Molecular determinants of state-dependent block of Na+ channels by local anesthetics. , 1994, Science.
[109] J. Balser,et al. Enhanced Na(+) channel intermediate inactivation in Brugada syndrome. , 2000, Circulation research.
[110] D. Roden,et al. Drug‐Induced J Point Elevation , 1999, Journal of cardiovascular electrophysiology.
[111] S. Priori,et al. Long QT syndrome patients with mutations of the SCN5A and HERG genes have differential responses to Na+ channel blockade and to increases in heart rate. Implications for gene-specific therapy. , 1995, Circulation.
[112] T. Scheuer,et al. A mutation in segment IVS6 disrupts fast inactivation of sodium channels. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[113] G. Tomaselli,et al. Topology of the P segments in the sodium channel pore revealed by cysteine mutagenesis. , 1997, Biophysical journal.
[114] S. Cannon,et al. The Position of the Fast-Inactivation Gate during Lidocaine Block of Voltage-gated Na+ Channels , 1999, The Journal of general physiology.
[115] C Antzelevitch,et al. Sodium channel block with mexiletine is effective in reducing dispersion of repolarization and preventing torsade des pointes in LQT2 and LQT3 models of the long-QT syndrome. , 1997, Circulation.
[116] J. Balser,et al. A Structural Rearrangement in the Sodium Channel Pore Linked to Slow Inactivation and Use Dependence , 2000, The Journal of general physiology.
[117] B. Khodorov,et al. Inhibition of sodium currents in frog ranvier node treated with local anesthetics Role of slow sodium inactivation , 1976 .
[118] 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.
[119] J. Makielski,et al. Lidocaine alters activation gating of cardiac Na channels , 2000, Pflügers Archiv.
[120] D. Hanck,et al. The Role of the Putative Inactivation Lid in Sodium Channel Gating Current Immobilization , 2000, The Journal of general physiology.
[121] E. Perozo,et al. Structural rearrangements underlying K+-channel activation gating. , 1999, Science.
[122] Y. Rudy,et al. Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia , 1999, Nature.
[123] B. Kerem,et al. Effects of flecainide in patients with new SCN5A mutation: mutation-specific therapy for long-QT syndrome? , 2000, Circulation.
[124] A. Wilde,et al. Cardiac conduction defects associate with mutations in SCN5A , 1999, Nature Genetics.