Y1767C, a novel SCN5A mutation, induces a persistent Na+ current and potentiates ranolazine inhibition of Nav1.5 channels.
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Mexiletine differentially restores the trafficking defects caused by two brugada syndrome mutationsNa⁺ transport in the normal and failing heart - remember the balanceProton-dependent inhibition of the cardiac sodium channel Nav1.5 by ranolazineDigenic inheritance novel mutations in SCN5a and SNTA1 increase late I(Na) contributing to LQT syndrome.Sodium overload due to a persistent current that attenuates the arrhythmogenic potential of a novel LQT3 mutationFluoxetine blocks Nav1.5 channels via a mechanism similar to that of class 1 antiarrhythmics.Gating pore currents are defects in common with two Nav1.5 mutations in patients with mixed arrhythmias and dilated cardiomyopathy.Functional characterization of a novel frameshift mutation in the C-terminus of the Nav1.5 channel underlying a Brugada syndrome with variable expression in a Spanish family.Treatment of cardiac arrhythmias in a mouse model of Rett syndrome with Na+-channel-blocking antiepileptic drugs.Altered physiological functions and ion currents in atrial fibroblasts from patients with chronic atrial fibrillation.Ranolazine: an antianginal drug with antiarrhythmic properties.Advances in targeting voltage-gated sodium channels with small molecules.Voltage-gated sodium channels: pharmaceutical targets via anticonvulsants to treat epileptic syndromes.Biophysical characterization of M1476I, a sodium channel founder mutation associated with cold-induced myotonia in French Canadians.MTSET modification of D4S6 cysteines stabilize the fast inactivated state of Nav1.5 sodium channels.Mutations in the Voltage Sensors of Domains I and II of Nav1.5 that are Associated with Arrhythmias and Dilated Cardiomyopathy Generate Gating Pore Currents.Effect of ovariectomy on intracellular Ca2+ regulation in guinea pig cardiomyocytes.The congenital long QT syndrome Type 3: An update.The efficacy of Ranolazine on E1784K is altered by temperature and calcium.Novel SCN5A mutations in two families with "Brugada-like" ST elevation in the inferior leads and conduction disturbances.
P2860
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P2860
Y1767C, a novel SCN5A mutation, induces a persistent Na+ current and potentiates ranolazine inhibition of Nav1.5 channels.
description
2010 nî lūn-bûn
@nan
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
2010年论文
@zh
2010年论文
@zh-cn
name
Y1767C, a novel SCN5A mutation ...... inhibition of Nav1.5 channels.
@en
Y1767C, a novel SCN5A mutation ...... inhibition of Nav1.5 channels.
@nl
type
label
Y1767C, a novel SCN5A mutation ...... inhibition of Nav1.5 channels.
@en
Y1767C, a novel SCN5A mutation ...... inhibition of Nav1.5 channels.
@nl
prefLabel
Y1767C, a novel SCN5A mutation ...... inhibition of Nav1.5 channels.
@en
Y1767C, a novel SCN5A mutation ...... inhibition of Nav1.5 channels.
@nl
P2093
P2860
P1476
Y1767C, a novel SCN5A mutation ...... inhibition of Nav1.5 channels.
@en
P2093
Carlo Napolitano
Michael E O'Leary
Mohamed Chahine
Silvia G Priori
P2860
P304
P356
10.1152/AJPHEART.00539.2010
P577
2010-11-12T00:00:00Z