Cellular consequences of HERG mutations in the long QT syndrome: precursors to sudden cardiac death.

doi:10.1016/s0008-6363(00)00293-5

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Article

Cellular consequences of HERG mutations in the long QT syndrome: precursors to sudden cardiac death.

Cardiovascular research - 1 May 2001

Clancy C E, Rudy Y

Abstract excerpt

BACKGROUND: A variety of mutations in HERG, the major subunit of the rapidly activating component of the cardiac delayed rectifier I(Kr), have been found to underlie the congenital Long-QT syndrome, LQT2. LQT2 may give rise to severe arrhythmogenic phenotypes leading to sudden cardiac death. OBJECTIVE: We attempt to elucidate the mechanisms by which heterogeneous LQT2 genotypes can lead to prolongation of the...

Topics

Action Potentials
Cation Transport Proteins
Computer Simulation
DNA-Binding Proteins
Death, Sudden, Cardiac
ERG1 Potassium Channel
Electrocardiography
Ether-A-Go-Go Potassium Channels
Humans
Long QT Syndrome
Markov Chains

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Models, Cardiovascular

Mutation

Potassium Channels

Potassium Channels, Voltage-Gated

Trans-Activators

Transcriptional Regulator ERG

Source

Open in PubMed

Identifiers

PMID: 11334834
DOI: 10.1016/s0008-6363(00)00293-5

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

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