ArticleThe Journal of general physiology2009
Dynamic coupling of voltage sensor and gate involved in closed-state inactivation of kv4.2 channels.
Article in The Journal of general physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 49 citations in OpenAlex.
- KChIP1 splice variants modulate Kv4 channels by promoting P/C-type inactivation features.Scientific reports · 2026Article
- Etiological involvement of KCND1 variants in an X-linked neurodevelopmental disorder with variable expressivity.American journal of human genetics · 2024Article
- Mono-allelic KCNB2 variants lead to a neurodevelopmental syndrome caused by altered channel inactivation.American journal of human genetics · 2024Article
- Article
- Neuronal Roles of the Multifunctional Protein Dipeptidyl Peptidase-like 6 (DPP6).International journal of molecular sciences · 2022Review
- Ionic Channels as Potential Targets for the Treatment of Autism Spectrum Disorder: A Review.Current neuropharmacology · 2022Review
- KCND2 variants associated with global developmental delay differentially impair Kv4.2 channel gating.Human molecular genetics · 2021Article
- Article
- Variation of Two S3b Residues in KFrontiers in pharmacology · 2021Article
- S4-S5 linker movement during activation and inactivation in voltage-gated KProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Kv4.2 autism and epilepsy mutation enhances inactivation of closed channels but impairs access to inactivated state after opening.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- β Subunits Functionally Differentiate Human Kv4.3 Potassium Channel Splice Variants.Frontiers in physiology · 2017Article
- Closed-state inactivation involving an internal gate in Kv4.1 channels modulates pore blockade by intracellular quaternary ammonium ions.Scientific reports · 2016Article
- Intra- and Intersubunit Dynamic Binding in Kv4.2 Channel Closed-State Inactivation.Biophysical journal · 2016Article
- Modulation of Closed-State Inactivation in Kv2.1/Kv6.4 Heterotetramers as Mechanism for 4-AP Induced Potentiation.PloS one · 2015Article
- Update on the implication of potassium channels in autism: K(+) channelautism spectrum disorder.Frontiers in cellular neuroscience · 2015Review
- Interfacial gating triad is crucial for electromechanical transduction in voltage-activated potassium channels.The Journal of general physiology · 2014Article
- Mechanisms of activation of voltage-gated potassium channels.Acta naturae · 2014Article
- The tetramerization domain potentiates Kv4 channel function by suppressing closed-state inactivation.Biophysical journal · 2014Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated potassium channels related to the Shal gene of Drosophila (Kv4 channels) mediate a subthreshold-activating current (I(SA)) that controls dendritic excitation and the backpropagation of action potentials in neurons. Kv4 channels also exhibit a prominent low voltage-induced closed-state inactivation, but the underlying molecular mechanism is poorly understood. Here, we examined a structural model in which dynamic coupling between the voltage sensors and the cytoplasmic gate underlies inactivation in Kv4.2 channels. We performed an alanine-scanning mutagenesis in the S4-S5 linker, the initial part of S5, and the distal part of S6 and functionally characterized the mutants under two-electrode voltage clamp in Xenopus oocytes. In a large fraction of the mutants (>80%) normal channel function was preserved, but the mutations influenced the likelihood of the channel to enter the closed-inactivated state. Depending on the site of mutation, low-voltage inactivation kinetics were slowed or accelerated, and the voltage dependence of steady-state inactivation was shifted positive or negative. Still, in some mutants these inactivation parameters remained unaffected. Double mutant cycle analysis based on kinetic and steady-state parameters of low-voltage inactivation revealed that residues known to be critical for voltage-dependent gate opening, including Glu 323 and Val 404, are also critical for Kv4.2 closed-state inactivation. Selective redox modulation of corresponding double-cysteine mutants supported the idea that these residues are involved in a dynamic coupling, which mediates both transient activation and closed-state inactivation in Kv4.2 channels.
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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.