Cardiac sodium channelopathies. - Wikidata - wikimedia - TriplyDB

Cardiac sodium channelopathies.

Cardiac sodium channelopathies.

http://www.wikidata.org/entity/Q33906972

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Mexiletine differentially restores the trafficking defects caused by two brugada syndrome mutations Inherited arrhythmias: The cardiac channelopathies Towards a Unified Theory of Calmodulin Regulation (Calmodulation) of Voltage-Gated Calcium and Sodium Channels Cellular hyper-excitability caused by mutations that alter the activation process of voltage-gated sodium channels Bisphenol A binds to the local anesthetic receptor site to block the human cardiac sodium channel Surface Electrocardiogram Predictors of Sudden Cardiac Arrest The role of the SCN5A-encoded channelopathy in irritable bowel syndrome and other gastrointestinal disorders Proton-dependent inhibition of the cardiac sodium channel Nav1.5 by ranolazine Cloning and expression of the two new variants of Nav1.5/SCN5A in rat brain Characterization of the honeybee AmNaV1 channel and tools to assess the toxicity of insecticides Genetic variants in SCN5A promoter are associated with arrhythmia phenotype severity in patients with heterozygous loss-of-function mutation Digenic 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 mutation Bimodal voltage dependence of TRPA1: mutations of a key pore helix residue reveal strong intrinsic voltage-dependent inactivation.Tetrodotoxin (TTX) as a therapeutic agent for pain.SCN5A mutations in Brugada syndrome are associated with increased cardiac dimensions and reduced contractility.A novel missense mutation, I890T, in the pore region of cardiac sodium channel causes Brugada syndrome Kinetic model of Nav1.5 channel provides a subtle insight into slow inactivation associated excitability in cardiac cells.A heterozygous deletion mutation in the cardiac sodium channel gene SCN5A with loss- and gain-of-function characteristics manifests as isolated conduction disease, without signs of Brugada or long QT syndrome.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.Novel heterozygous mutation c.4282G>T in the SCN5A gene in a family with Brugada syndrome Concomitant Brugada-like and short QT electrocardiogram linked to SCN5A mutation A novel NaV1.5 voltage sensor mutation associated with severe atrial and ventricular arrhythmias.Assessment of the Risk Factors and Outcomes for Postoperative Atrial Fibrillation Patients Undergoing Isolated Coronary Artery Bypass Grafting.Breaking down protein degradation mechanisms in cardiac muscle.The cardiomyocyte molecular clock, regulation of Scn5a, and arrhythmia susceptibility.Cardiac sodium channel mutations: why so many phenotypes?Early afterdepolarizations in cardiac myocytes: beyond reduced repolarization reserve FGF13 modulates the gating properties of the cardiac sodium channel Nav1.5 in an isoform-specific manner.FGF12 is a candidate Brugada syndrome locus.Biallelic SCN10A mutations in neuromuscular disease and epileptic encephalopathy.Genetic analysis of cardiac SCN5A Gene in Iranian patients with hereditary cardiac arrhythmias.Cardiac Channelopathies and Sudden Death: Recent Clinical and Genetic Advances Redox control of cardiac excitability.Advances in targeting voltage-gated sodium channels with small molecules.Long QT syndrome: beyond the causal mutation.Induced pluripotent stem cells as cardiac arrhythmic in vitro models and the impact for drug discovery.Saxitoxin.Biophysics, pathophysiology, and pharmacology of ion channel gating pores.

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P2860

Cardiac sodium channelopathies.

http://www.wikidata.org/entity/Q33906972

description

2009 nî lūn-bûn

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2009 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2009 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

Cardiac sodium channelopathies.

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Cardiac sodium channelopathies.

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Cardiac sodium channelopathies.

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Cardiac sodium channelopathies.

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Cardiac sodium channelopathies.

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Cardiac sodium channelopathies.

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Ahmad S Amin

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Alaleh Asghari-Roodsari

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Hanno L Tan

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P2860

Cardiac conduction defects associate with mutations in SCN5A

Novel mechanism for sudden infant death syndrome: persistent late sodium current secondary to mutations in caveolin-3

Mutation in glycerol-3-phosphate dehydrogenase 1 like gene (GPD1-L) decreases cardiac Na+ current and causes inherited arrhythmias

Syntrophin mutation associated with long QT syndrome through activation of the nNOS-SCN5A macromolecular complex

Mutant caveolin-3 induces persistent late sodium current and is associated with long-QT syndrome

Sodium channel β1 subunit mutations associated with Brugada syndrome and cardiac conduction disease in humans

SCN4B-encoded sodium channel beta4 subunit in congenital long-QT syndrome

SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome

Gain-of-function mutation of Nav1.5 in atrial fibrillation enhances cellular excitability and lowers the threshold for action potential firing

Mutations in sodium channel β1- and β2-subunits associated with atrial fibrillation

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