Characterization of human cardiac Na+ channel mutations in the congenital long QT syndrome. - Wikidata - awgldk - TriplyDB

Characterization of human cardiac Na+ channel mutations in the congenital long QT syndrome.

Characterization of human cardiac Na+ channel mutations in the congenital long QT syndrome.

http://www.wikidata.org/entity/Q36689783

about

alpha-1-syntrophin mutation and the long-QT syndrome: a disease of sodium channel disruption Conduction abnormalities and ventricular arrhythmogenesis: The roles of sodium channels and gap junctions The role of late I Na in development of cardiac arrhythmias Cardiac sodium channel Nav1.5 mutations and cardiac arrhythmia Regulation of intracellular Na(+) in health and disease: pathophysiological mechanisms and implications for treatment The late Na+ current--origin and pathophysiological relevance Towards a Unified Theory of Calmodulin Regulation (Calmodulation) of Voltage-Gated Calcium and Sodium Channels Human iPS cell model of type 3 long QT syndrome recapitulates drug-based phenotype correction Sodium channel β subunits: emerging targets in channelopathies SCN5A variant that blocks fibroblast growth factor homologous factor regulation causes human arrhythmia Channel cytoplasmic loops alter voltage-dependent sodium channel activation in an isoform-specific manner Residue-specific effects on slow inactivation at V787 in D2-S6 of Na(v)1.4 sodium channels.Mutations in Danish patients with long QT syndrome and the identification of a large founder family with p.F29L in KCNH2.Inherited long QT syndromes: a paradigm for understanding arrhythmogenesis.A novel SCN5A mutation associated with long QT-3: altered inactivation kinetics and channel dysfunction.A common SCN5A polymorphism modulates the biophysical effects of an SCN5A mutation.Characterization of the cardiac sodium channel SCN5A mutation, N1325S, in single murine ventricular myocytes.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 death Diversity of mammalian voltage-gated sodium channels.Inherited disorders of voltage-gated sodium channels.Cardiac sodium channelopathies.Interaction between the sodium channel inactivation linker and domain III S4-S5.Novel SCN5A mutation in amiodarone-responsive multifocal ventricular ectopy-associated cardiomyopathy.Channelopathies: ion channel defects linked to heritable clinical disorders.Congenital long QT syndromes and Brugada syndrome: the arrhythmogenic ion channel disorders.An EF-hand in the sodium channel couples intracellular calcium to cardiac excitability.A revised view of cardiac sodium channel "blockade" in the long-QT syndrome Impact of gene patents and licensing practices on access to genetic testing for long QT syndrome.Monogenic atrial fibrillation as pathophysiological paradigms.Genetic disorders of neuromuscular ion channels.Cardiac sodium channel diseases.The long QT interval is not only inherited but is also linked to cardiac hypertrophy.Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels Pharmacogenomics of cardiovascular complications in diabetes and obesity.Ion channels: function unravelled by dysfunction.Na(+) channel mutation that causes both Brugada and long-QT syndrome phenotypes: a simulation study of mechanism.Sodium channel inactivation: molecular determinants and modulation.Sodium channel inactivation is altered by substitution of voltage sensor positive charges Bradycardia-mediated ventricular electrical remodeling.The role of late I and antiarrhythmic drugs in EAD formation and termination in Purkinje fibers.

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P2860

Characterization of human cardiac Na+ channel mutations in the congenital long QT syndrome.

http://www.wikidata.org/entity/Q36689783

description

1996 nî lūn-bûn

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1996年の論文

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1996年論文

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1996年論文

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1996年論文

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1996年論文

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1996年論文

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1996年论文

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1996年论文

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1996年论文

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name

Characterization of human card ...... e congenital long QT syndrome.

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Characterization of human card ...... e congenital long QT syndrome.

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type

label

Characterization of human card ...... e congenital long QT syndrome.

@ast

Characterization of human card ...... e congenital long QT syndrome.

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Characterization of human card ...... e congenital long QT syndrome.

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Characterization of human card ...... e congenital long QT syndrome.

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PNAS.93.23.13200

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Characterization of human card ...... e congenital long QT syndrome.

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P2093

A L George

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

D W Wang

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K Yazawa

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P B Bennett

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P2860

Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches

A molecular basis for cardiac arrhythmia: HERG mutations cause long QT syndrome

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

Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels.

Primary structure and functional expression of the human cardiac tetrodotoxin-insensitive voltage-dependent sodium channel

Primary structure of the adult human skeletal muscle voltage-dependent sodium channel

The long Q-T syndrome.

Molecular mechanism for an inherited cardiac arrhythmia.

Evidence of genetic heterogeneity in Romano-Ward long QT syndrome. Analysis of 23 families.

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.

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13200-13205

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10.1073/PNAS.93.23.13200

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24070

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