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Article

Loss-of-function mutations of the K+ channel gene KCNJ2 constitute a rare cause of long QT syndrome

23 Jul 2004

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Share to Cardiac electrophysiology and arrhythmias
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 15276028
DOI: 10.1016/j.yjmcc.2004.05.011

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Loss-of-function mutations of the K+ channel gene KCNJ2 constitute a rare cause of long QT syndromePMID 15276028Read ↗

Novel mutation in the KCNH2 gene associated with long QT syndrome.Semantic proximity Read ↗

Large-scale mutational analysis of Kv11.1 reveals molecular insights into type 2 long QT syndromeSemantic proximity Read ↗

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Characterization of a novel KCNJ2 sequence variant detected in Andersen-Tawil syndrome patients.Semantic proximity Read ↗

Non-missense variants ofKCNH2show better outcomes in type 2 long QT syndromeSemantic proximity Read ↗

Molecular pathogenesis of long QT syndrome type 2Semantic proximity Read ↗

Long QT Syndrome Type 2: Emerging Strategies for Correcting Class 2 KCNH2 (hERG) Mutations and Identifying New PatientsSemantic proximity Read ↗

Loss-of-function mutations in cardiac ryanodine receptor channel cause various types of arrhythmias including long QT syndrome.Semantic proximity Read ↗

Identification of a KCNE2 Gain-of-Function Mutation in Patients with Familial Atrial FibrillationSemantic proximity Read ↗

Human RyR2 (Ryanodine Receptor 2) Loss-of-Function Mutations: Clinical Phenotypes and In Vitro Characterization.Semantic proximity Read ↗

KCNQ2 related-epilepsy: Report of nine cases and novel loss-of-function missense variantsSemantic proximity Read ↗

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