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Articles related to 18616619 [Unique ID], provided by the PubMed system
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Zhang Y, Wang T, Ma A, et al. 
CORRELATIONS BETWEEN CLINICAL AND PHYSIOLOGICAL CONSEQUENCES OF THE NOVEL MUTATION R878C IN A HIGHLY CONSERVED PORE RESIDUE IN THE CARDIAC NA(+) CHANNEL. [JOURNAL ARTICLE]
Acta Physiol (Oxf) 2008 Jun 24.
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Keller DI, Acharfi S, Delacrétaz E, et al. 
A novel mutation in SCN5A, delQKP 1507-1509, causing long QT syndrome: role of Q1507 residue in sodium channel inactivation. [Journal Article]
J Mol Cell Cardiol 2003 Dec; 35(12):1513-21.
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Baroudi G, Acharfi S, Larouche C, et al. 
Expression and intracellular localization of an SCN5A double mutant R1232W/T1620M implicated in Brugada syndrome. [Journal Article]
Circ Res 2002 Jan 11; 90(1):E11-6.
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Casini S, Tan HL, Bhuiyan ZA, et al. 
Characterization of a novel SCN5A mutation associated with Brugada syndrome reveals involvement of DIIIS4-S5 linker in slow inactivation. [JOURNAL ARTICLE]
Cardiovasc Res 2007 Aug 22.
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Shin DJ, Kim E, Park SB, et al. 
A novel mutation in the SCN5A gene is associated with Brugada syndrome. [JOURNAL ARTICLE]
Life Sci 2006 Nov 30.
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Smits JP, Koopmann TT, Wilders R, et al. 
A mutation in the human cardiac sodium channel (E161K) contributes to sick sinus syndrome, conduction disease and Brugada syndrome in two families. [Journal Article]
J Mol Cell Cardiol 2005 Jun; 38(6):969-81.
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Keller DI, Rougier JS, Kucera JP, et al. 
Brugada syndrome and fever: genetic and molecular characterization of patients carrying SCN5A mutations. [Journal Article]
Cardiovasc Res 2005 Aug 15; 67(3):510-9.
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Vilin YY, Fujimoto E, Ruben PC 
A single residue differentiates between human cardiac and skeletal muscle Na+ channel slow inactivation. [Journal Article]
Biophys J 2001 May; 80(5):2221-30.
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Wehrens XH, Rossenbacker T, Jongbloed RJ, et al. 
A novel mutation L619F in the cardiac Na+ channel SCN5A associated with long-QT syndrome (LQT3): a role for the I-II linker in inactivation gating. [Journal Article]
Hum Mutat 2003 May; 21(5):552.
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