Defective cardiac ion channels: from mutations to clinical syndromes (Q34977359)

5 August 2017

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title

Defective cardiac ion channels: from mutations to clinical syndromes (English)

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5 August 2017

Colleen E Clancy

1

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5 August 2017

Robert S Kass

series ordinal

2

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5 August 2017

language of work or name

English

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publication date

1 October 2002

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Journal of Clinical Investigation

5 August 2017

published in

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5 August 2017

volume

110

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5 August 2017

issue

8

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5 August 2017

page(s)

1075-1077

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Long QT syndrome, Brugada syndrome, and conduction system disease are linked to a single sodium channel mutation

5 August 2017

cites work

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Regulation of ryanodine receptors via macromolecular complexes: a novel role for leucine/isoleucine zippers

8 July 2018

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Ionic current basis of electrocardiographic waveforms: a model study

8 July 2018

1 reference

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Na(+) channel mutation that causes both Brugada and long-QT syndrome phenotypes: a simulation study of mechanism

8 July 2018

1 reference

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Variable expression of long QT syndrome among gene carriers from families with five different HERG mutations

8 July 2018

1 reference

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A mutant cardiac sodium channel with multiple biophysical defects associated with overlapping clinical features of Brugada syndrome and cardiac conduction disease

8 July 2018

1 reference

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Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channel

8 July 2018

1 reference

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Novel SCN5A mutation leading either to isolated cardiac conduction defect or Brugada syndrome in a large French family

8 July 2018

1 reference

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Phosphorylation-dependent regulation of ryanodine receptors: a novel role for leucine/isoleucine zippers

8 July 2018

1 reference

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A sodium-channel mutation causes isolated cardiac conduction disease

8 July 2018

1 reference

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Enhanced Na(+) channel intermediate inactivation in Brugada syndrome

8 July 2018

1 reference

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A single Na(+) channel mutation causing both long-QT and Brugada syndromes

8 July 2018

1 reference

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Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent

8 July 2018

1 reference

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Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation

8 July 2018

1 reference

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Slow conduction in cardiac tissue, I: effects of a reduction of excitability versus a reduction of electrical coupling on microconduction.

8 July 2018

1 reference

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Genetic basis and molecular mechanism for idiopathic ventricular fibrillation

8 July 2018

1 reference

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Long QT syndrome patients with mutations of the SCN5A and HERG genes have differential responses to Na+ channel blockade and to increases in heart rate. Implications for gene-specific therapy.

8 July 2018

1 reference

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Molecular mechanism for an inherited cardiac arrhythmia

8 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=150807

Ionic bases for electrophysiological distinctions among epicardial, midmyocardial, and endocardial myocytes from the free wall of the canine left ventricle

8 July 2018

1 reference

12 December 2020

Ionic mechanisms of propagation in cardiac tissue. Roles of the sodium and L-type calcium currents during reduced excitability and decreased gap junction coupling

1 reference

12 December 2020

Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia

1 reference

12 December 2020

Two distinct congenital arrhythmias evoked by a multidysfunctional Na(+) channel

1 reference

12 December 2020

Inherited Brugada and long QT-3 syndrome mutations of a single residue of the cardiac sodium channel confer distinct channel and clinical phenotypes

1 reference

12 December 2020

Identifiers

DOI

10.1172/JCI0216945

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5 August 2017

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5 August 2017

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