Papers associated with scn5a

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	Molecular mechanism for an inherited cardiac arrhythmia., Bennett PB, Yazawa K, Makita N, George AL., Nature. August 24, 1995; 376 (6542): 683-5.
	A de novo missense mutation of human cardiac Na+ channel exhibiting novel molecular mechanisms of long QT syndrome., Makita N, Shirai N, Nagashima M, Matsuoka R, Yamada Y, Tohse N, Kitabatake A., FEBS Lett. February 13, 1998; 423 (1): 5-9.
	Phenotypic characterization of a novel long-QT syndrome mutation (R1623Q) in the cardiac sodium channel., Kambouris NG, Nuss HB, Johns DC, Tomaselli GF, Marban E, Balser JR., Circulation. February 24, 1998; 97 (7): 640-4.
	Genetic basis and molecular mechanism for idiopathic ventricular fibrillation., Chen Q, Kirsch GE, Zhang D, Brugada R, Brugada J, Brugada P, Potenza D, Moya A, Borggrefe M, Breithardt G, Ortiz-Lopez R, Wang Z, Antzelevitch C, O'Brien RE, Schulze-Bahr E, Keating MT, Towbin JA, Wang Q., Nature. March 19, 1998; 392 (6673): 293-6.
	Congenital long-QT syndrome caused by a novel mutation in a conserved acidic domain of the cardiac Na+ channel., Wei J, Wang DW, Alings M, Fish F, Wathen M, Roden DM, George AL., Circulation. June 22, 1999; 99 (24): 3165-71.
	Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome., Rook MB, Bezzina Alshinawi C, Groenewegen WA, van Gelder IC, van Ginneken AC, Jongsma HJ, Mannens MM, Wilde AA., Cardiovasc Res. December 1, 1999; 44 (3): 507-17.
	A single Na(+) channel mutation causing both long-QT and Brugada syndromes., Bezzina C, Veldkamp MW, van Den Berg MP, Postma AV, Rook MB, Viersma JW, van Langen IM, Tan-Sindhunata G, Bink-Boelkens MT, van Der Hout AH, Mannens MM, Wilde AA., Circ Res. December 1, 1999; 85 (12): 1206-13.
	SCN5A mutation (T1620M) causing Brugada syndrome exhibits different phenotypes when expressed in Xenopus oocytes and mammalian cells., Baroudi G, Carbonneau E, Pouliot V, Chahine M., FEBS Lett. February 4, 2000; 467 (1): 12-6.
	A revised view of cardiac sodium channel "blockade" in the long-QT syndrome., Kambouris NG, Nuss HB, Johns DC, Marbán E, Tomaselli GF, Balser JR., J Clin Invest. April 1, 2000; 105 (8): 1133-40.
	Functional suppression of sodium channels by beta(1)-subunits as a molecular mechanism of idiopathic ventricular fibrillation., Wan X, Wang Q, Kirsch GE., J Mol Cell Cardiol. October 1, 2000; 32 (10): 1873-84.
	Novel mechanism for Brugada syndrome: defective surface localization of an SCN5A mutant (R1432G)., Baroudi G, Pouliot V, Denjoy I, Guicheney P, Shrier A, Chahine M., Circ Res. June 22, 2001; 88 (12): E78-83.
	The sodium channel beta-subunit SCN3b modulates the kinetics of SCN5a and is expressed heterogeneously in sheep heart., Fahmi AI, Patel M, Stevens EB, Fowden AL, John JE, Lee K, Pinnock R, Morgan K, Jackson AP, Vandenberg JI., J Physiol. December 15, 2001; 537 (Pt 3): 693-700.
	Genetic and biophysical basis of sudden unexplained nocturnal death syndrome (SUNDS), a disease allelic to Brugada syndrome., Vatta M, Dumaine R, Varghese G, Richard TA, Shimizu W, Aihara N, Nademanee K, Brugada R, Brugada J, Veerakul G, Li H, Bowles NE, Brugada P, Antzelevitch C, Towbin JA., Hum Mol Genet. February 1, 2002; 11 (3): 337-45.
	Novel mutations in domain I of SCN5A cause Brugada syndrome., Vatta M, Dumaine R, Antzelevitch C, Brugada R, Li H, Bowles NE, Nademanee K, Brugada J, Brugada P, Towbin JA., Mol Genet Metab. April 1, 2002; 75 (4): 317-24.
	Cocaine binds to a common site on open and inactivated human heart (Na(v)1.5) sodium channels., O'Leary ME, Chahine M., J Physiol. June 15, 2002; 541 (Pt 3): 701-16.
	A cardiac sodium channel mutation cosegregates with a rare connexin40 genotype in familial atrial standstill., Groenewegen WA, Firouzi M, Bezzina CR, Vliex S, van Langen IM, Sandkuijl L, Smits JP, Hulsbeek M, Rook MB, Jongsma HJ, Wilde AA., Circ Res. January 10, 2003; 92 (1): 14-22.
	Compound heterozygosity for mutations (W156X and R225W) in SCN5A associated with severe cardiac conduction disturbances and degenerative changes in the conduction system., Bezzina CR, Rook MB, Groenewegen WA, Herfst LJ, van der Wal AC, Lam J, Jongsma HJ, Wilde AA, Mannens MM., Circ Res. February 7, 2003; 92 (2): 159-68.
	Serum and glucocorticoid inducible kinases in the regulation of the cardiac sodium channel SCN5A., Boehmer C, Wilhelm V, Palmada M, Wallisch S, Henke G, Brinkmeier H, Cohen P, Pieske B, Lang F., Cardiovasc Res. March 15, 2003; 57 (4): 1079-84.
	A novel LQT3 mutation implicates the human cardiac sodium channel domain IVS6 in inactivation kinetics., Groenewegen WA, Bezzina CR, van Tintelen JP, Hoorntje TM, Mannens MM, Wilde AA, Jongsma HJ, Rook MB., Cardiovasc Res. March 15, 2003; 57 (4): 1072-8.
	Na+ channel mutation leading to loss of function and non-progressive cardiac conduction defects., Herfst LJ, Potet F, Bezzina CR, Groenewegen WA, Le Marec H, Hoorntje TM, Demolombe S, Baró I, Escande D, Jongsma HJ, Wilde AA, Rook MB., J Mol Cell Cardiol. May 1, 2003; 35 (5): 549-57.
	Closing and inactivation potentiate the cocaethylene inhibition of cardiac sodium channels by distinct mechanisms., O'Leary ME, Digregorio M, Chahine M., Mol Pharmacol. December 1, 2003; 64 (6): 1575-85.
	A cardiac sodium channel mutation identified in Brugada syndrome associated with atrial standstill., Takehara N, Makita N, Kawabe J, Sato N, Kawamura Y, Kitabatake A, Kikuchi K., J Intern Med. January 1, 2004; 255 (1): 137-42.
	Compound mutations: a common cause of severe long-QT syndrome., Westenskow P, Splawski I, Timothy KW, Keating MT, Sanguinetti MC., Circulation. April 20, 2004; 109 (15): 1834-41.
	Occurrence of a tetrodotoxin-sensitive calcium current in rat ventricular myocytes after long-term myocardial infarction., Alvarez JL, Salinas-Stefanon E, Orta G, Ferrer T, Talavera K, Galán L, Vassort G., Cardiovasc Res. September 1, 2004; 63 (4): 653-61.
	State-dependent trapping of flecainide in the cardiac sodium channel., Ramos E, O'leary ME., J Physiol. October 1, 2004; 560 (Pt 1): 37-49.
	Identification and characterisation of a novel KCNQ1 mutation in a family with Romano-Ward syndrome., Zehelein J, Thomas D, Khalil M, Wimmer AB, Koenen M, Licka M, Wu K, Kiehn J, Brockmeier K, Kreye VA, Karle CA, Katus HA, Ulmer HE, Schoels W., Biochim Biophys Acta. November 5, 2004; 1690 (3): 185-92.
	Molecular basis of the mammalian potency of the scorpion alpha-like toxin, BmK M1., Liu LH, Bosmans F, Maertens C, Zhu RH, Wang DC, Tytgat J., FASEB J. April 1, 2005; 19 (6): 594-6.
	OD1, the first toxin isolated from the venom of the scorpion Odonthobuthus doriae active on voltage-gated Na+ channels., Jalali A, Bosmans F, Amininasab M, Clynen E, Cuypers E, Zaremirakabadi A, Sarbolouki MN, Schoofs L, Vatanpour H, Tytgat J., FEBS Lett. August 1, 2005; 579 (19): 4181-6.
	Four novel tarantula toxins as selective modulators of voltage-gated sodium channel subtypes., Bosmans F, Rash L, Zhu S, Diochot S, Lazdunski M, Escoubas P, Tytgat J., Mol Pharmacol. February 1, 2006; 69 (2): 419-29.
	GLUT8 is dispensable for embryonic development but influences hippocampal neurogenesis and heart function., Membrez M, Hummler E, Beermann F, Haefliger JA, Savioz R, Pedrazzini T, Thorens B., Mol Cell Biol. June 1, 2006; 26 (11): 4268-76.
	Differential sensitivity of rat voltage-sensitive sodium channel isoforms to pyrazoline-type insecticides., Silver KS, Soderlund DM., Toxicol Appl Pharmacol. July 15, 2006; 214 (2): 209-17.
	The intracellular domain of the beta 2 subunit modulates the gating of cardiac Na v 1.5 channels., Zimmer T, Benndorf K., Biophys J. June 1, 2007; 92 (11): 3885-92.
	Solution structure of Jingzhaotoxin-III, a peptide toxin inhibiting both Nav1.5 and Kv2.1 channels., Liao Z, Yuan C, Peng K, Xiao Y, Liang S., Toxicon. July 1, 2007; 50 (1): 135-43.
	Structure/function characterization of micro-conotoxin KIIIA, an analgesic, nearly irreversible blocker of mammalian neuronal sodium channels., Zhang MM, Green BR, Catlin P, Fiedler B, Azam L, Chadwick A, Terlau H, McArthur JR, French RJ, Gulyas J, Rivier JE, Smith BJ, Norton RS, Olivera BM, Yoshikami D, Bulaj G., J Biol Chem. October 19, 2007; 282 (42): 30699-706.
	Cardiac sodium channel gene variants and sudden cardiac death in women., Albert CM, Nam EG, Rimm EB, Jin HW, Hajjar RJ, Hunter DJ, MacRae CA, Ellinor PT., Circulation. January 1, 2008; 117 (1): 16-23.
	Cardiac sodium channel mutation in atrial fibrillation., Ellinor PT, Nam EG, Shea MA, Milan DJ, Ruskin JN, MacRae CA., Heart Rhythm. January 1, 2008; 5 (1): 99-105.
	Combination of cardiac conduction disease and long QT syndrome caused by mutation T1620K in the cardiac sodium channel., Surber R, Hensellek S, Prochnau D, Werner GS, Benndorf K, Figulla HR, Zimmer T., Cardiovasc Res. March 1, 2008; 77 (4): 740-8.
	An extracellular Cu2+ binding site in the voltage sensor of BK and Shaker potassium channels., Ma Z, Wong KY, Horrigan FT., J Gen Physiol. May 1, 2008; 131 (5): 483-502.
	Cardiac ion channel gene mutations in sudden infant death syndrome., Otagiri T, Kijima K, Osawa M, Ishii K, Makita N, Matoba R, Umetsu K, Hayasaka K., Pediatr Res. November 1, 2008; 64 (5): 482-7.
	Correlations between clinical and physiological consequences of the novel mutation R878C in a highly conserved pore residue in the cardiac Na+ channel., Zhang Y, Wang T, Ma A, Zhou X, Gui J, Wan H, Shi R, Huang C, Grace AA, Huang CL, Trump D, Zhang H, Zimmer T, Lei M., Acta Physiol (Oxf). December 1, 2008; 194 (4): 311-23.
	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, Ma JH, Zhang PH, Xing JL., Acta Pharmacol Sin. March 1, 2010; 31 (3): 297-306.
	Multiple loss-of-function mechanisms contribute to SCN5A-related familial sick sinus syndrome., Gui J, Wang T, Jones RP, Trump D, Zimmer T, Lei M., PLoS One. June 7, 2010; 5 (6): e10985.
	Pharmacological modulation of brain Nav1.2 and cardiac Nav1.5 subtypes by the local anesthetic ropivacaine., Cheng HW, Yang HT, Zhou JJ, Ji YH, Zhu HY., Neurosci Bull. August 1, 2010; 26 (4): 289-96.
	Induction of vertebrate regeneration by a transient sodium current., Tseng AS, Beane WS, Lemire JM, Masi A, Levin M., J Neurosci. September 29, 2010; 30 (39): 13192-200.
	Molecular mechanism of allosteric modification of voltage-dependent sodium channels by local anesthetics., Arcisio-Miranda M, Muroi Y, Chowdhury S, Chanda B., J Gen Physiol. November 1, 2010; 136 (5): 541-54.
	Extracellular proton modulation of the cardiac voltage-gated sodium channel, Nav1.5., Jones DK, Peters CH, Tolhurst SA, Claydon TW, Ruben PC., Biophys J. November 2, 2011; 101 (9): 2147-56.
	A proton leak current through the cardiac sodium channel is linked to mixed arrhythmia and the dilated cardiomyopathy phenotype., Gosselin-Badaroudine P, Keller DI, Huang H, Pouliot V, Chatelier A, Osswald S, Brink M, Chahine M., PLoS One. January 1, 2012; 7 (5): e38331.
	JZTX-XIII, a Kv channel gating modifier toxin from Chinese tarantula Chilobrachys jingzhao., Yuan C, Liu Z, Hu W, Gao T, Liang S., Toxicon. February 1, 2012; 59 (2): 265-71.
	18β-Glycyrrhetinic acid preferentially blocks late Na current generated by ΔKPQ Nav1.5 channels., Du YM, Xia CK, Zhao N, Dong Q, Lei M, Xia JH., Acta Pharmacol Sin. June 1, 2012; 33 (6): 752-60.
	Coexisting mutations/polymorphisms of the long QT syndrome genes in patients with repaired Tetralogy of Fallot are associated with the risks of life-threatening events., Chiu SN, Wu MH, Su MJ, Wang JK, Lin MT, Chang CC, Hsu HW, Shen CT, Thériault O, Chahine M., Hum Genet. August 1, 2012; 131 (8): 1295-304.

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