Overlap syndrome of cardiac sodium channel disease in mice carrying the equivalent mutation of human SCN5A-1795insD
about
Dissection of a quantitative trait locus for PR interval duration identifies Tnni3k as a novel modulator of cardiac conductionSodium channel β1 subunit mutations associated with Brugada syndrome and cardiac conduction disease in humansCorrelations between clinical and physiological consequences of the novel mutation R878C in a highly conserved pore residue in the cardiac Na+ channelScn3b knockout mice exhibit abnormal ventricular electrophysiological propertiesThe role of late I Na in development of cardiac arrhythmiasCardiac sodium channel Nav1.5 mutations and cardiac arrhythmiaThe cardiac sodium channel displays differential distribution in the conduction system and transmural heterogeneity in the murine ventricular myocardiumCommon variants at SCN5A-SCN10A and HEY2 are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac deathHomocysteine enriched diet leads to prolonged QT interval and reduced left ventricular performance in telemetric monitored mice.The cardiac sodium channel mutation delQKP 1507-1509 is associated with the expanding phenotypic spectrum of LQT3, conduction disorder, dilated cardiomyopathy, and high incidence of youth sudden deathTorsades de pointes during complete atrioventricular block: Genetic factors and electrocardiogram correlates.Voltage-independent sodium channels emerge for an expression of activity-induced spontaneous spikes in GABAergic neuronsStructure-based assessment of disease-related mutations in human voltage-gated sodium channels.Vascular Endothelial Growth Factor-B Induces a Distinct Electrophysiological Phenotype in Mouse Heart.Re-evaluation of the action potential upstroke velocity as a measure of the Na+ current in cardiac myocytes at physiological conditions.Autonomic modulation and antiarrhythmic therapy in a model of long QT syndrome type 3Optimizing catecholaminergic polymorphic ventricular tachycardia therapy in calsequestrin-mutant miceA 50% reduction of excitability but not of intercellular coupling affects conduction velocity restitution and activation delay in the mouse heart.Deletion of FoxO1 leads to shortening of QRS by increasing Na(+) channel activity through enhanced expression of both cardiac NaV1.5 and β3 subunitSCN5A mutations in Brugada syndrome are associated with increased cardiac dimensions and reduced contractility.Recent progress in congenital long QT syndromeDeletion of PDK1 causes cardiac sodium current reduction in miceStriking In vivo phenotype of a disease-associated human SCN5A mutation producing minimal changes in vitroIntracellular Ca2+ release underlies the development of phase 2 in mouse ventricular action potentials.Altered sinoatrial node function and intra-atrial conduction in murine gain-of-function Scn5a+/ΔKPQ hearts suggest an overlap syndrome.Reduced Na(+) and higher K(+) channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice.Induced pluripotent stem cell derived cardiomyocytes as models for cardiac arrhythmias.Gap junction remodeling and cardiac arrhythmogenesis in a murine model of oculodentodigital dysplasia.Knockin animal models of inherited arrhythmogenic diseases: what have we learned from them?The tight junction protein CAR regulates cardiac conduction and cell-cell communication.Gene mutations in cardiac arrhythmias: a review of recent evidence in ion channelopathies.The primary arrhythmia syndromes: same mutation, different manifestations. Are we starting to understand why?Myocyte necrosis underlies progressive myocardial dystrophy in mouse dsg2-related arrhythmogenic right ventricular cardiomyopathy.Essential role of axonal VGSC inactivation in time-dependent deceleration and unreliability of spike propagation at cerebellar Purkinje cells.Exome Sequencing Identifies Compound Heterozygous Mutations in SCN5A Associated with Congenital Complete Heart Block in the Thai Population.Founder mutations in the Netherlands: SCN5a 1795insD, the first described arrhythmia overlap syndrome and one of the largest and best characterised families worldwide.Mouse Models of SCN5A-Related Cardiac ArrhythmiasPathophysiological Mechanisms of Sino-Atrial Dysfunction and Ventricular Conduction Disease Associated with SCN5A Deficiency: Insights from Mouse Models.An introduction to murine models of atrial fibrillationLate sodium current inhibition in acquired and inherited ventricular (dys)function and arrhythmias.
P2860
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P2860
Overlap syndrome of cardiac sodium channel disease in mice carrying the equivalent mutation of human SCN5A-1795insD
description
2006 nî lūn-bûn
@nan
2006 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@ast
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@en
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@nl
type
label
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@ast
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@en
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@nl
prefLabel
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@ast
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@en
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@nl
P2093
P50
P1433
P1476
Overlap syndrome of cardiac so ...... tation of human SCN5A-1795insD
@en
P2093
Antoni C G van Ginneken
Arie O Verkerk
Carol Ann Remme
Charly N W Belterman
Connie R Bezzina
Dieter Nuyens
Hanno L Tan
Jacques M T de Bakker
Marian A van Roon
Marieke W Veldkamp
P304
P356
10.1161/CIRCULATIONAHA.106.653949
P407
P577
2006-12-12T00:00:00Z