ArticleHeart rhythm2015
Microscopic mechanisms for long QT syndrome type 1 revealed by single-channel analysis of I(Ks) with S3 domain mutations in KCNQ1.
Article in Heart rhythm, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- A physiologically-relevant intermediate state structure of a voltage-gated potassium channel.Nature communications · 2025Article
- Structural and electrophysiological basis for the modulation of KCNQ1 channel currents by ML277.Nature communications · 2022Article
- Predicting the functional impact of KCNQ1 variants with artificial neural networks.PLoS computational biology · 2022Article
- ML277 regulates KCNQ1 single-channel amplitudes and kinetics, modified by voltage sensor state.The Journal of general physiology · 2021Article
- Gating and Regulation of KCNQ1 and KCNQ1 + KCNE1 Channel Complexes.Frontiers in physiology · 2020Review
- Article
- The IBiophysical journal · 2018Article
- Mechanisms Underlying the Dual Effect of Polyunsaturated Fatty Acid Analogs on Kv7.1.Cell reports · 2018Article
- Mechanisms of KCNQ1 channel dysfunction in long QT syndrome involving voltage sensor domain mutations.Science advances · 2018Article
- Single channel kinetic analysis of the cAMP effect on IChannels (Austin, Tex.) · 2018Article
- cAMP-dependent regulation ofThe Journal of general physiology · 2017Article
- Photo-Cross-Linking of IBiophysical journal · 2017Article
- KCNQ1 p.L353L affects splicing and modifies the phenotype in a founder population with long QT syndrome type 1.Journal of medical genetics · 2017Article
- Molecular Pathophysiology of Congenital Long QT Syndrome.Physiological reviews · 2017Review
- Article
- Understanding the microscopic mechanisms for LQT1 needs a global view of the I(Ks) channel.Heart rhythm · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe slowly activating delayed rectifier current IKs participates in cardiac repolarization, particularly at high heart rates, and mutations in this K(+) channel complex underlie long QT syndrome (LQTS) types 1 and 5.
objectiveThe purpose of this study was to determine biophysical mechanisms of LQT1 through single-channel kinetic analysis of IKs carrying LQT1 mutations in the S3 transmembrane region of the pore-forming subunit KCNQ1.
methodsWe analyzed cell-attached recordings from mammalian cells in which a single active KCNQ1 (wild type or mutant) and KCNE1 complex could be detected.
resultsThe S3 mutants of KCNQ1 studied (D202H, I204F, V205M, and S209F), with the exception of S209F, all led to a reduction in channel activity through distinct kinetic mechanisms. D202H, I204F, and V205M showed decreased open probability (Po) compared with wild type (0.07, 0.04, and 0.12 vs 0.2); increased first latency from 1.66 to >2 seconds at +60 mV (I204F, V205M); variable-to-severe reductions in open dwell times (≥50% in V205M); stabilization of closed states (D202H); and an inability of channels to reach full conductance levels (V205M, I204F). S209F is a kinetic gain-of-function mutation with a high Po (0.40) and long open-state dwell times.
conclusionS3 mutations in KCNQ1 cause diverse kinetic defects in I(Ks), affecting opening and closing properties, and can account for LQT1 phenotypes.
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