ArticleBiophysical journal2008
Mechanism of the modulation of Kv4:KChIP-1 channels by external K+.
Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 29 citations in OpenAlex.
- KChIP1 splice variants modulate Kv4 channels by promoting P/C-type inactivation features.Scientific reports · 2026Article
- A broad survey of choanoflagellates revises the evolutionary history of the Shaker family of voltage-gated KProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Estradiol Enhances the Depolarizing Response to GABA and AMPA Synaptic Conductances in Arcuate Kisspeptin Neurons by Diminishing Voltage-Gated Potassium Currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Propofol inhibits prokaryotic voltage-gated NaThe Journal of general physiology · 2018Article
- A-Type KFrontiers in molecular neuroscience · 2018Review
- Article
- 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
- Zebrafish CaV2.1 calcium channels are tailored for fast synchronous neuromuscular transmission.Biophysical journal · 2015Article
- Kv3.4 channel function and dysfunction in nociceptors.Channels (Austin, Tex.) · 2015Article
- Modulatory mechanisms and multiple functions of somatodendritic A-type K (+) channel auxiliary subunits.Frontiers in cellular neuroscience · 2014Review
- Modeling-independent elucidation of inactivation pathways in recombinant and native A-type Kv channels.The Journal of general physiology · 2012Article
- Voltage sensor inactivation in potassium channels.Frontiers in pharmacology · 2012Article
- Mechanisms of closed-state inactivation in voltage-gated ion channels.The Journal of physiology · 2011Review
- A novel N-terminal motif of dipeptidyl peptidase-like proteins produces rapid inactivation of KV4.2 channels by a pore-blocking mechanism.Channels (Austin, Tex.) · 2009Article
- Dynamic coupling of voltage sensor and gate involved in closed-state inactivation of kv4.2 channels.The Journal of general physiology · 2009Article
- Kv4 Channels Underlie the Subthreshold-Operating A-type K-current in Nociceptive Dorsal Root Ganglion Neurons.Frontiers in molecular neuroscience · 2009Article
- Dynamic, nonlinear feedback regulation of slow pacemaking by A-type potassium current in ventral tegmental area neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Kv4 accessory protein DPPX (DPP6) is a critical regulator of membrane excitability in hippocampal CA1 pyramidal neurons.Journal of neurophysiology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In response to a prolonged membrane depolarization, inactivation autoregulates the activity of voltage-gated ion channels. Slow inactivation involving a localized constriction of the selectivity filter (P/C-type mechanism) is prevalent in many voltage-gated K(+) channels of the Kv1 subfamily. However, the generalization of this mechanism to other Kv channel subfamilies has remained uncertain and controversial. In agreement with a "foot-in-the-door" mechanism and the presence of ion-ion interactions in the pore, elevated external K(+) slows the development of P/C-type inactivation and accelerates its recovery. In sharp contrast and resembling the regulation of the hippocampal A-type K(+) current, we found that Kv4.x channels associated with KChIP-1 (an auxiliary subunit) exhibit accelerated inactivation and unaffected recovery from inactivation when exposed to elevated external K(+). This regulation depends on the ability of a permeant ion to enter the selectivity filter (K(+) = Rb(+) = NH4(+) > Cs(+) > Na(+)); and the apparent equilibrium dissociation constant of a single regulatory site is 8 mM for K(+). By applying a robust quantitative global kinetic modeling approach to all macroscopic properties over a 210-mV range of membrane potentials, we determined that elevated external K(+) inhibits unstable closed states outside the main activation pathway and thereby promotes preferential closed-state inactivation. These results suggest the presence of a vestigial and unstable P/C-type mechanism of inactivation in Kv4 channels and strengthen the concept of novel mechanisms of closed-state inactivation. Regulation of Kv4 channel inactivation by hyperkalemia may help to explain the pathophysiology of electrolyte imbalances in excitable tissues.
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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.