A novel rare variant in SCN1Bb linked to Brugada syndrome and SIDS by combined modulation of Na(v)1.5 and K(v)4.3 channel currents. - Wikidata - awgldk - TriplyDB

A novel rare variant in SCN1Bb linked to Brugada syndrome and SIDS by combined modulation of Na(v)1.5 and K(v)4.3 channel currents.

A novel rare variant in SCN1Bb linked to Brugada syndrome and SIDS by combined modulation of Na(v)1.5 and K(v)4.3 channel currents.

http://www.wikidata.org/entity/Q35907195

about

Channelopathies from mutations in the cardiac sodium channel protein complex Sudden unexplained death in infants and children: the role of undiagnosed inherited cardiac conditions J-wave syndromes: Brugada and early repolarization syndromes On the multiple roles of the voltage gated sodium channel β1 subunit in genetic diseases Sodium channel β subunits: emerging targets in channelopathies Abnormal repolarization as the basis for late potentials and fractionated electrograms recorded from epicardium in experimental models of Brugada syndrome.Enhanced risk profiling of implanted defibrillator shocks with circulating SCN5A mRNA splicing variants: a pilot trial.Brugada syndrome risk loci seem protective against atrial fibrillation.J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge Assigning cause for sudden unexpected infant death.Novel heterozygous mutation c.4282G>T in the SCN5A gene in a family with Brugada syndrome The Role of Pharmacogenetics in Atrial Fibrillation Therapeutics: Is Personalized Therapy in Sight?Cardiac ion channelopathies and the sudden infant death syndrome Brugada Syndrome: Clinical, Genetic, Molecular, Cellular, and Ionic Aspects.Spectrum and prevalence of mutations involving BrS1- through BrS12-susceptibility genes in a cohort of unrelated patients referred for Brugada syndrome genetic testing: implications for genetic testing.Cellular and ionic mechanisms underlying the effects of cilostazol, milrinone, and isoproterenol to suppress arrhythmogenesis in an experimental model of early repolarization syndrome.The genetic component of Brugada syndrome Novel Therapeutic Strategies for the Management of Ventricular Arrhythmias Associated with the Brugada Syndrome Cellular mechanisms underlying the effects of milrinone and cilostazol to suppress arrhythmogenesis associated with Brugada syndrome.Unfolded protein response regulates cardiac sodium current in systolic human heart failure Atrial fibrillation: the role of common and rare genetic variants.Modulatory mechanisms and multiple functions of somatodendritic A-type K (+) channel auxiliary subunits SCN1B gene variants in Brugada Syndrome: a study of 145 SCN5A-negative patients Current perspectives in genetic cardiovascular disorders: from basic to clinical aspects.KCNE4 and KCNE5: K(+) channel regulation and cardiac arrhythmogenesis.Histone Deacetylase Inhibitors Prolong Cardiac Repolarization through Transcriptional Mechanisms.Mechanisms of noncovalent β subunit regulation of NaV channel gating.A missense mutation in the sodium channel β2 subunit reveals SCN2B as a new candidate gene for Brugada syndrome.Sudden cardiac death in the young: how can disease recognition and prevention in family members be improved?Investigations of the Navβ1b sodium channel subunit in human ventricle; functional characterization of the H162P Brugada syndrome mutant.Regulation of Cardiac Voltage-Gated Sodium Channel by Kinases: Roles of Protein Kinases A and C.Voltage-Gated Sodium Channel β Subunits and Their Related Diseases.Scn1b deletion leads to increased tetrodotoxin-sensitive sodium current, altered intracellular calcium homeostasis and arrhythmias in murine hearts.Infant sudden death: Mutations responsible for impaired Nav1.5 channel trafficking and function.Sudden infant death syndrome and inherited cardiac conditions.Cardiac channelopathies associated with infantile fatal ventricular arrhythmias: from the cradle to the bench.KV4.3 Expression Modulates NaV1.5 Sodium Current.J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge.Voltage-Gated Sodium Channel β1/β1B Subunits Regulate Cardiac Physiology and Pathophysiology.Functional implications of a rare variant in the sodium channel β1B subunit (SCN1B) in a 5-month-old male sudden infant death syndrome case.

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P2860

A novel rare variant in SCN1Bb linked to Brugada syndrome and SIDS by combined modulation of Na(v)1.5 and K(v)4.3 channel currents.

http://www.wikidata.org/entity/Q35907195

description

2011 nî lūn-bûn

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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2011年论文

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2011年论文

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name

A novel rare variant in SCN1Bb ...... and K(v)4.3 channel currents.

@ast

A novel rare variant in SCN1Bb ...... and K(v)4.3 channel currents.

@en

type

label

A novel rare variant in SCN1Bb ...... and K(v)4.3 channel currents.

@ast

A novel rare variant in SCN1Bb ...... and K(v)4.3 channel currents.

@en

prefLabel

A novel rare variant in SCN1Bb ...... and K(v)4.3 channel currents.

@ast

A novel rare variant in SCN1Bb ...... and K(v)4.3 channel currents.

@en

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J.HRTHM.2011.12.006

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A novel rare variant in SCN1Bb ...... and K(v)4.3 channel currents.

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Aintzane Alday

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Christian Veltmann

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Dan Hu

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David J Tester

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Gabriel Caceres

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Hector Barajas-Martínez

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Janire Urrutia

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Michael J Ackerman

http://www.w3.org/2001/XMLSchema#string

Oscar Casis

http://www.w3.org/2001/XMLSchema#string

P2860

Loss-of-function mutation of the SCN3B-encoded sodium channel {beta}3 subunit associated with a case of idiopathic ventricular fibrillation

Molecular cloning and functional expression of the human sodium channel beta1B subunit, a novel splicing variant of the beta1 subunit

Sudden infant death syndrome-associated mutations in the sodium channel beta subunits

Mutations in sodium channel β-subunit SCN3B are associated with early-onset lone atrial fibrillation

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

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

Transient outward current (I(to)) gain-of-function mutations in the KCND3-encoded Kv4.3 potassium channel and Brugada syndrome

Sodium channel beta subunits mediate homophilic cell adhesion and recruit ankyrin to points of cell-cell contact

Modulation of Kv4.3 current by accessory subunits

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10.1016/J.HRTHM.2011.12.006

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Charles Antzelevitch

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