Gain-of-function KCNH2 mutations in patients with Brugada syndrome.

doi:10.1111/jce.12361

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Article

Gain-of-function KCNH2 mutations in patients with Brugada syndrome.

Journal of cardiovascular electrophysiology - 1 May 2014

Wang Q I, Ohno Seiko, Ding Wei-Guang, Fukuyama Megumi, Miyamoto Akashi, Itoh Hideki, Makiyama Takeru, Wu Jie, Bai Jiayu, Hasegawa Kanae, Shinohara Tetsuji, Takahashi Naohiko, Shimizu Akihiko, Matsuura Hiroshi, Horie Minoru

Abstract excerpt

BACKGROUND: Brugada syndrome (BrS) is an inherited disease characterized by right precordial ST segment elevation on electrocardiograms (ECGs) that predisposes patients to sudden cardiac death as a result of polymorphic ventricular tachyarrhythmia or ventricular fibrillation (VF). In BrS patients, except for SCN5A, mutations in other responsible genes are poorly elucidated. METHODS AND RESULTS: We identified 4...

Topics

Action Potentials
Adult
Animals
Brugada Syndrome
CHO Cells
Calcium Channels, L-Type
Cricetulus
DNA Mutational Analysis
ERG1 Potassium Channel
Electrocardiography

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Ether-A-Go-Go Potassium Channels

Genetic Predisposition to Disease

Genetic Testing

Humans

Kinetics

Male

Middle Aged

Mutation

Source

Open in PubMed

Identifiers

PMID: 24400717
DOI: 10.1111/jce.12361

Genes

KCNH2

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-24400717-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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