ArticlePloS one2009
Functional interactions between KCNE1 C-terminus and the KCNQ1 channel.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Functions of the KCNE Gene Family in Ion Channels.Biochemical genetics · 2026Review
- Functional Profiling ofCirculation. Genomic and precision medicine · 2025Article
- Identification of KCNE6, a new member of the KCNE family of potassium channel auxiliary subunits.Communications biology · 2024Article
- Association of the P441L KCNQ1 variant with severity of long QT syndrome and risk of cardiac events.Frontiers in cardiovascular medicine · 2022Article
- The ERG1 KFrontiers in molecular neuroscience · 2022Review
- Long QT syndrome - Bench to bedside.Heart rhythm O2 · 2021Article
- Physical and functional interaction sites in cytoplasmic domains of KCNQ1 and KCNE1 channel subunits.American journal of physiology. Heart and circulatory physiology · 2020Article
- A conserved arginine/lysine-based motif promotes ER export of KCNE1 and KCNE2 to regulate KCNQ1 channel activity.Channels (Austin, Tex.) · 2019Article
- The IBiophysical journal · 2018Article
- KCNE1 and KCNE3 modulate KCNQ1 channels by affecting different gating transitions.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Molecular Pathophysiology of Congenital Long QT Syndrome.Physiological reviews · 2017Review
- Structural basis for KCNE3 modulation of potassium recycling in epithelia.Science advances · 2016Article
- Electrophysiological properties of iPS cell-derived cardiomyocytes from a patient with long QT syndrome type 1 harboring the novel mutation M437V of KCNQ1.Regenerative therapy · 2016Article
- Review
- Differential modulations of KCNQ1 by auxiliary proteins KCNE1 and KCNE2.Scientific reports · 2014Article
- Dysfunctional potassium channel subunit interaction as a novel mechanism of long QT syndrome.Heart rhythm · 2013Article
- KCNE genetics and pharmacogenomics in cardiac arrhythmias: much ado about nothing?Expert review of clinical pharmacology · 2013Review
- Wide spectrum of inhibitory effects of sertraline on cardiac ion channels.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2012Article
- The KCNE Tango - How KCNE1 Interacts with Kv7.1.Frontiers in pharmacology · 2012Article
- Regulation of Voltage-Activated K(+) Channel Gating by Transmembrane β Subunits.Frontiers in pharmacology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The KCNE1 gene product (minK protein) associates with the cardiac KvLQT1 potassium channel (encoded by KCNQ1) to create the cardiac slowly activating delayed rectifier, I(Ks). Mutations throughout both genes are linked to the hereditary cardiac arrhythmias in the Long QT Syndrome (LQTS). KCNE1 exerts its specific regulation of KCNQ1 activation via interactions between membrane-spanning segments of the two proteins. Less detailed attention has been focused on the role of the KCNE1 C-terminus in regulating channel behavior. We analyzed the effects of an LQT5 point mutation (D76N) and the truncation of the entire C-terminus (Delta70) on channel regulation, assembly and interaction. Both mutations significantly shifted voltage dependence of activation in the depolarizing direction and decreased I(Ks) current density. They also accelerated rates of channel deactivation but notably, did not affect activation kinetics. Truncation of the C-terminus reduced the apparent affinity of KCNE1 for KCNQ1, resulting in impaired channel formation and presentation of KCNQ1/KCNE1 complexes to the surface. Complete saturation of KCNQ1 channels with KCNE1-Delta70 could be achieved by relative over-expression of the KCNE subunit. Rate-dependent facilitation of K(+) conductance, a key property of I(Ks) that enables action potential shortening at higher heart rates, was defective for both KCNE1 C-terminal mutations, and may contribute to the clinical phenotype of arrhythmias triggered by heart rate elevations during exercise in LQTS mutations. These results support several roles for KCNE1 C-terminus interaction with KCNQ1: regulation of channel assembly, open-state destabilization, and kinetics of channel deactivation.
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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.