Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

hERG1a/1b heteromeric currents exhibit amplified attenuation of inactivation in variant 1 short QT syndrome.

Biochemical and biophysical research communications - 14 Aug 2009

McPate M J, Zhang H, Cordeiro J M, Dempsey C E, Witchel H J, Hancox J C

Abstract excerpt

Potassium channels encoded by hERG (human ether-à-go-go-related gene) underlie the cardiac rapid delayed rectifier K+ current (IKr) and hERG mutations underpin clinically important repolarization disorders. Virtually all electrophysiological investigations of hERG mutations have studied exclusively the hERG1a isoform; however, recent evidence indicates that native IKr channels may be comprised of hERG1a together...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Arrhythmias, Cardiac
Share to Cell Line

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to ERG1 Potassium Channel

Share to Ether-A-Go-Go Potassium Channels

Share to Mutation

Source

Open in PubMed Open full text

Identifiers

PMID: 19501051
DOI: 10.1016/j.bbrc.2009.05.134
PMCID: PMC2708341

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

hERG1a/1b heteromeric currents exhibit amplified attenuation of inactivation in variant 1 short QT syndrome.PMID 19501051Read ↗

Biophysical characterization of the short QT mutation hERG-N588K reveals a mixed gain-and loss-of-function.Semantic proximity Read ↗

hERG 1a LQT2 C-terminus truncation mutants display hERG 1b-dependent dominant negative mechanisms.Semantic proximity Read ↗

Isoform-specific dominant-negative effects associated with hERG1 G628S mutation in long QT syndrome.Semantic proximity Read ↗

Action potential clamp and pharmacology of the variant 1 Short QT Syndrome T618I hERG K⁺ channel.Semantic proximity Read ↗

Concerted all-or-none subunit interactions mediate slow deactivation of human ether-à-go-go-related gene K+ channels.Semantic proximity Read ↗

Modulation of I(Kr) inactivation by mutation N588K in KCNH2: a link to arrhythmogenesis in short QT syndrome.Semantic proximity Read ↗

hERG K(+) channels: structure, function, and clinical significance.Semantic proximity Read ↗

The variant hERG/R148W associated with LQTS is a mutation that reduces current density on co-expression with the WT.Semantic proximity Read ↗

Comparative effects of the short QT N588K mutation at 37 degrees C on hERG K+ channel current during ventricular, Purkinje fibre and atrial action potentials: an action potential clamp study.Semantic proximity Read ↗

A novel form of short QT syndrome (SQT3) is caused by a mutation in the KCNJ2 gene.Semantic proximity Read ↗

A K+ Channel Splice Variant Common in Human Heart Lacks a C-terminal Domain Required for Expression of Rapidly Activating Delayed Rectifier CurrentSemantic proximity Read ↗

Long QT syndrome-associated mutations in the Per-Arnt-Sim (PAS) domain of HERG potassium channels accelerate channel deactivation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.