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

Functional Knockout of the Transient Outward Current, Long-QT Syndrome, and Cardiac Remodeling in Mice Expressing a Dominant-Negative Kv4 α Subunit

7 Sept 1998

Abstract excerpt

A novel in vivo experimental strategy, involving cell type-specific expression of a dominant-negative K+ channel pore-forming alpha subunit, was developed and exploited to probe the molecular identity of the cardiac transient outward K+ current (I(to)). A point mutation (W to F) was introduced at position 362 in the pore region of Kv4.2 to produce a nonconducting mutant (Kv4.2W362F) subunit. Coexpression of...

Read the complete abstract on PubMed

Topics

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

Share to Cardiac electrophysiology and arrhythmias
Share to Ion channel regulation and function
Share to Neuroscience and Neuropharmacology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 9734479
DOI: 10.1161/01.res.83.5.560

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Functional Knockout of the Transient Outward Current, Long-QT Syndrome, and Cardiac Remodeling in Mice Expressing a Dominant-Negative Kv4 α SubunitPMID 9734479Read ↗

Functional consequences of elimination of i(to,f) and i(to,s): early afterdepolarizations, atrioventricular block, and ventricular arrhythmias in mice lacking Kv1.4 and expressing a dominant-negative Kv4 alpha subunit.Semantic proximity Read ↗

Targeted expression of a dominant-negative K(v)4.2 K(+) channel subunit in the mouse heart.Semantic proximity Read ↗

A defect in the Kv channel-interacting protein 2 (KChIP2) gene leads to a complete loss of I(to) and confers susceptibility to ventricular tachycardia.Semantic proximity Read ↗

In vivo effect of a dominant negative Kv4.2 loss-of-function mutation eliminating I(to,f) on atrial refractoriness and atrial fibrillation in mice.Semantic proximity Read ↗

Knockdown of the TRPM4 channel alters cardiac electrophysiology and hemodynamics in a sex- and age-dependent manner in miceSemantic proximity Read ↗

Functional role of inward rectifier current in heart probed by Kir2.1 overexpression and dominant-negative suppression.Semantic proximity Read ↗

Electrical remodeling and arrhythmias in long-QT syndrome: lessons from genetic models in mice.Semantic proximity Read ↗

Kv4.3 is not required for the generation of functional Ito,f channels in adult mouse ventricles.Semantic proximity Read ↗

The Kir2.1E299V mutation increases atrial fibrillation vulnerability while protecting the ventricles against arrhythmias in a mouse model of short QT syndrome type 3.Semantic proximity Read ↗

The consequences of disrupting cardiac inwardly rectifying K(+) current (I(K1)) as revealed by the targeted deletion of the murine Kir2.1 and Kir2.2 genes.Semantic proximity Read ↗

Dual Dysfunction of Kir2.1 Underlies Conduction and Excitation-Contraction Coupling Defects Promoting Arrhythmias in a Mouse Model of Andersen-Tawil Syndrome Type 1Semantic proximity Read ↗

Loss of K+ currents in heart failure is accentuated in KChIP2 deficient mice.Semantic proximity Read ↗

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