Long QT syndrome: cellular basis and arrhythmia mechanism in LQT2.

doi:10.1046/j.1540-8167.2000.01413.x

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Article

Long QT syndrome: cellular basis and arrhythmia mechanism in LQT2.

Journal of cardiovascular electrophysiology - 1 Dec 2000

January C T, Gong Q, Zhou Z

Abstract excerpt

LQT2 is one form of the congenital long QT syndrome. It results from mutations in the human ether-a-go-go-related gene (HERG), and more than 80 mutations, usually causing single amino acid substitutions in the HERG protein, are known. HERG encodes the ion channel pore-forming subunit protein for the rapidly activating delayed rectifier K+ channel (I(Kr)) in the heart. This review summarizes current findings about...

Topics

Amino Acid Substitution
Arrhythmias, Cardiac
Cation Transport Proteins
DNA-Binding Proteins
ERG1 Potassium Channel
Ether-A-Go-Go Potassium Channels
Genes, Dominant
Humans
Long QT Syndrome
Mutation
Potassium

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Potassium Channels

Potassium Channels, Voltage-Gated

Protein Transport

Temperature

Trans-Activators

Transcriptional Regulator ERG

Source

Open in PubMed

Identifiers

PMID: 11196567
DOI: 10.1046/j.1540-8167.2000.01413.x

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 31 Aug 2026.

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