ArticleThe EMBO journal2009
Intracellular domains interactions and gated motions of I(KS) potassium channel subunits.
Article in The EMBO journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Functional Profiling ofCirculation. Genomic and precision medicine · 2025Article
- Predicting the Damaging Potential of UncharacterizedInternational journal of molecular sciences · 2025Article
- Arrhythmia-associated calmodulin variants interact with KCNQ1 to confer aberrant membrane trafficking and function.PNAS nexus · 2023Article
- Disruption of a Conservative Motif in the C-Terminal Loop of the KCNQ1 Channel Causes LQT Syndrome.International journal of molecular sciences · 2022Article
- HumanJournal of neurophysiology · 2022Article
- The unconventional biogenesis of Kv7.1-KCNE1 complexes.Science advances · 2020Article
- Physical and functional interaction sites in cytoplasmic domains of KCNQ1 and KCNE1 channel subunits.American journal of physiology. Heart and circulatory physiology · 2020Article
- The IBiophysical journal · 2018Article
- A Calmodulin C-Lobe CaNeuron · 2018Article
- Single channel kinetic analysis of the cAMP effect on IChannels (Austin, Tex.) · 2018Article
- CaChannels (Austin, Tex.) · 2017Article
- cAMP-dependent regulation ofThe Journal of general physiology · 2017Article
- Competition of calcified calmodulin N lobe and PIP2 to an LQT mutation site in Kv7.1 channel.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Molecular Pathophysiology of Congenital Long QT Syndrome.Physiological reviews · 2017Review
- Voltage-Dependent Gating: Novel Insights from KCNQ1 Channels.Biophysical journal · 2016Review
- Article
- LQT1 mutations in KCNQ1 C-terminus assembly domain suppress IKs using different mechanisms.Cardiovascular research · 2014Article
- Long QT mutations at the interface between KCNQ1 helix C and KCNE1 disrupt I(KS) regulation by PKA and PIP₂.Journal of cell science · 2014Article
- Differential modulations of KCNQ1 by auxiliary proteins KCNE1 and KCNE2.Scientific reports · 2014Article
- [Ca2+]i elevation and oxidative stress induce KCNQ1 protein translocation from the cytosol to the cell surface and increase slow delayed rectifier (IKs) in cardiac myocytes.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated K(+) channels co-assemble with auxiliary beta subunits to form macromolecular complexes. In heart, assembly of Kv7.1 pore-forming subunits with KCNE1 beta subunits generates the repolarizing K(+) current I(KS). However, the detailed nature of their interface remains unknown. Mutations in either Kv7.1 or KCNE1 produce the life-threatening long or short QT syndromes. Here, we studied the interactions and voltage-dependent motions of I(KS) channel intracellular domains, using fluorescence resonance energy transfer combined with voltage-clamp recording and in vitro binding of purified proteins. The results indicate that the KCNE1 distal C-terminus interacts with the coiled-coil helix C of the Kv7.1 tetramerization domain. This association is important for I(KS) channel assembly rules as underscored by Kv7.1 current inhibition produced by a dominant-negative C-terminal domain. On channel opening, the C-termini of Kv7.1 and KCNE1 come close together. Co-expression of Kv7.1 with the KCNE1 long QT mutant D76N abolished the K(+) currents and gated motions. Thus, during channel gating KCNE1 is not static. Instead, the C-termini of both subunits experience molecular motions, which are disrupted by the D76N causing disease mutation.
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