ArticleThe Journal of physiology2013
Stabilization of Kv4 protein by the accessory K(+) channel interacting protein 2 (KChIP2) subunit is required for the generation of native myocardial fast transient outward K(+) currents.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- KCells · 2023Review
- Control of Biophysical and Pharmacological Properties of Potassium Channels by Ancillary Subunits.Handbook of experimental pharmacology · 2021Article
- Differential Expression and Remodeling of Transient Outward Potassium Currents in Human Left Ventricles.Circulation. Arrhythmia and electrophysiology · 2018Article
- Notch signaling modulates the electrical behavior of cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2018Article
- Article
- Early remodeling of repolarizing KJournal of molecular and cellular cardiology · 2017Article
- KChIP2 regulates the cardiac Ca2+ transient and myocyte contractility by targeting ryanodine receptor activity.PloS one · 2017Article
- KChIP2 genotype dependence of transient outward current (Ito) properties in cardiomyocytes isolated from male and female mice.PloS one · 2017Article
- Notch-Mediated Epigenetic Regulation of Voltage-Gated Potassium Currents.Circulation research · 2016Article
- Transmural gradients in ion channel and auxiliary subunit expression.Progress in biophysics and molecular biology · 2016Review
- Potassium Channel Interacting Protein 2 (KChIP2) is not a transcriptional regulator of cardiac electrical remodeling.Scientific reports · 2016Article
- Molecular Basis of Functional Myocardial Potassium Channel Diversity.Cardiac electrophysiology clinics · 2016Review
- Reductions in the Cardiac Transient Outward K+ Current Ito Caused by Chronic β-Adrenergic Receptor Stimulation Are Partly Rescued by Inhibition of Nuclear Factor κB.The Journal of biological chemistry · 2016Article
- Myocardial KChIP2 Expression in Guinea Pig Resolves an Expanded Electrophysiologic Role.PloS one · 2016Article
- Kcne4 deletion sex- and age-specifically impairs cardiac repolarization in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- New insights into the complex effects of KChIP2 on calcium transients.American journal of physiology. Heart and circulatory physiology · 2015Article
- Transient outward potassium channel: a heart failure mediator.Heart failure reviews · 2015Review
- Article
- Mouse models of arrhythmogenic cardiovascular disease: challenges and opportunities.Current opinion in pharmacology · 2014Review
- A novel computational model of mouse myocyte electrophysiology to assess the synergy between Na+ loading and CaMKII.The Journal of physiology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The fast transient outward K(+) current (Ito,f) underlies the early phase of myocardial action potential repolarization, contributing importantly to the coordinated propagation of activity in the heart and to the generation of normal cardiac rhythms. Native Ito,f channels reflect the tetrameric assembly of Kv4 pore-forming (α) subunits, and previous studies suggest roles for accessory and regulatory proteins in controlling the cell surface expression and the biophysical properties of Kv4-encoded Ito,f channels. Here, we demonstrate that the targeted deletion of the cytosolic accessory subunit, K(+) channel interacting protein 2 (KChIP2), results in the complete loss of the Kv4.2 protein, the α subunit critical for the generation of mouse ventricular Ito,f. Expression of the Kcnd2 (Kv4.2) transcript in KChIP2(-/-) ventricles, however, is unaffected. The loss of the Kv4.2 protein results in the elimination of Ito,f in KChIP2(-/-) ventricular myocytes. In parallel with the elimination of Ito,f, the slow transient outward K(+) current (Ito,s) is upregulated and voltage-gated Ca(2+) currents (ICa,L) are decreased. In addition, surface electrocardiograms and ventricular action potential waveforms in KChIP2(-/-) and wild-type mice are not significantly different, suggesting that the upregulation of Ito,s and the reduction in ICa,L compensate for the loss of Ito,f. Additional experiments revealed that Ito,f is not 'rescued' by adenovirus-mediated expression of KChIP2 in KChIP2(-/-) myocytes, although ICa,L densities are increased. Taken together, these results demonstrate that association with KChIP2 early in the biosynthetic pathway and KChIP2-mediated stabilization of Kv4 protein are critical determinants of native cardiac Ito,f channel expression.
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