ArticleHeart rhythm2010
KCNE2 modulation of Kv4.3 current and its potential role in fatal rhythm disorders.
Article in Heart rhythm, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 28 citations in OpenAlex.
- KCNE gene family: From basic functions to diseases.Genes & diseases · 2026Review
- Voltage-dependent potassium channel regulatory subunits in the immune system.Biophysical reviews · 2026Review
- Review
- Cisplatin Neurotoxicity Targets Specific Subpopulations and KFrontiers in cellular neuroscience · 2022Article
- Recognition and clinical implications of high prevalence of migraine in patients with Brugada syndrome and drug-induced type 1 Brugada pattern.Journal of cardiovascular electrophysiology · 2020Article
- Disease-linked mutations alter the stoichiometries of HCN-KCNE2 complexes.Scientific reports · 2019Article
- Targeted next generation sequencing in a young population with suspected inherited malignant cardiac arrhythmias.European journal of human genetics : EJHG · 2018Article
- Kv4.3 Modulates the Distribution of hERG.Scientific reports · 2017Article
- Arrhythmogenic KCNE gene variants: current knowledge and future challenges.Frontiers in genetics · 2014Review
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Authors and funding
18 authors at 10 institutions in 5 countries.
Funding
Abstract
backgroundThe transient outward current I(to) is of critical importance in regulating myocardial electrical properties during the very early phase of the action potential. The auxiliary beta subunit KCNE2 recently was shown to modulate I(to).
objectiveThe purpose of this study was to examine the contributions of KCNE2 and its two published variants (M54T, I57T) to I(to).
methodsThe functional interaction between Kv4.3 (alpha subunit of human I(to)) and wild-type (WT), M54T, and I57T KCNE2, expressed in a heterologous cell line, was studied using patch-clamp techniques.
resultsCompared to expression of Kv4.3 alone, co-expression of WT KCNE2 significantly reduced peak current density, slowed the rate of inactivation, and caused a positive shift of voltage dependence of steady-state inactivation curve. These modifications rendered Kv4.3 channels more similar to native cardiac I(to). Both M54T and I57T variants significantly increased I(to) current density and slowed the inactivation rate compared with WT KCNE2. Moreover, both variants accelerated the recovery from inactivation.
conclusionThe study results suggest that KCNE2 plays a critical role in the normal function of the native I(to) channel complex in human heart and that M54T and I57T variants lead to a gain of function of I(to), which may contribute to generating potential arrhythmogeneity and pathogenesis for inherited fatal rhythm disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.