ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
The sodium channel accessory subunit Navβ1 regulates neuronal excitability through modulation of repolarizing voltage-gated K⁺ channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 89 citations in OpenAlex.
- Beyond the Alpha Subunit: Pharmacological Modulation of Kv4.2 Channels by Ancillary Proteins.Cells · 2026Review
- A Novel Mouse Model for Developmental and Epileptic Encephalopathy by Purkinje Cell-Specific Deletion ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Ataxia and cerebellar hypoexcitability in a mouse model of SCN1B-linked Dravet syndrome.JCI insight · 2025Article
- Altered cardiac excitability and arrhythmia in models of SCN1B-linked developmental and epileptic encephalopathy.JCI insight · 2025Article
- A spatial single-cell atlas of the claustro-insular region uncovers key regulators of neuronal identity and excitability.Nature communications · 2025Article
- Article
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- Developmental exposure of zebrafish to saxitoxin causes altered expression of genes associated with axonal growth.Neurotoxicology · 2024Article
- Implications of Lead (Pb)-Induced Transcriptomic and Phenotypic Alterations in the Aged Zebrafish (Toxics · 2024Article
- Complex Synaptic and Intrinsic Interactions Disrupt Input/Output Functions in the Hippocampus ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Epilepsy and sudden unexpected death in epilepsy in a mouse model of humanBrain communications · 2023Article
- SCN1B Genetic Variants: A Review of the Spectrum of Clinical Phenotypes and a Report of Early Myoclonic Encephalopathy.Children (Basel, Switzerland) · 2022Review
- Sodium channel β1 subunits participate in regulated intramembrane proteolysis-excitation coupling.JCI insight · 2021Article
- Proteomic and functional mapping of cardiac NaV1.5 channel phosphorylation sites.The Journal of general physiology · 2021Article
- SUMOylation of the Kv4.2 Ternary Complex Increases Surface Expression and Current Amplitude by Reducing Internalization in HEK 293 Cells.Frontiers in molecular neuroscience · 2021Article
- Voltage Gated Sodium Channel Genes in Epilepsy: Mutations, Functional Studies, and Treatment Dimensions.Frontiers in neurology · 2021Review
- Excitatory and inhibitory neuron defects in a mouse model of Scn1b-linked EIEE52.Annals of clinical and translational neurology · 2020Article
- Sodium channel β1 subunits are post-translationally modified by tyrosine phosphorylation,The Journal of biological chemistry · 2020Article
- Cell-Adhesion Properties of β-Subunits in the Regulation of Cardiomyocyte Sodium Channels.Biomolecules · 2020Review
- Up-regulation of voltage-gated sodium channels by peptides mimicking S4-S5 linkers reveals a variation of the ligand-receptor mechanism.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The channel pore-forming α subunit Kv4.2 is a major constituent of A-type (I(A)) potassium currents and a key regulator of neuronal membrane excitability. Multiple mechanisms regulate the properties, subcellular targeting, and cell-surface expression of Kv4.2-encoded channels. In the present study, shotgun proteomic analyses of immunoprecipitated mouse brain Kv4.2 channel complexes unexpectedly identified the voltage-gated Na⁺ channel accessory subunit Navβ1. Voltage-clamp and current-clamp recordings revealed that knockdown of Navβ1 decreases I(A) densities in isolated cortical neurons and that action potential waveforms are prolonged and repetitive firing is increased in Scn1b-null cortical pyramidal neurons lacking Navβ1. Biochemical and voltage-clamp experiments further demonstrated that Navβ1 interacts with and increases the stability of the heterologously expressed Kv4.2 protein, resulting in greater total and cell-surface Kv4.2 protein expression and in larger Kv4.2-encoded current densities. Together, the results presented here identify Navβ1 as a component of native neuronal Kv4.2-encoded I(A) channel complexes and a novel regulator of I(A) channel densities and neuronal excitability.
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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.