ArticleProceedings of the National Academy of Sciences of the United States of America2012
Modulation of voltage-gated K+ channels by the sodium channel β1 subunit.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 76 citations in OpenAlex.
- 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
- Altered cardiac excitability and arrhythmia in models of SCN1B-linked developmental and epileptic encephalopathy.JCI insight · 2025Article
- Ataxia and cerebellar hypoexcitability in a mouse model of SCN1B-linked Dravet syndrome.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
- 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
- "Fifth-day fits" revisited: A literature review of benign idiopathic neonatal seizures and comparison with KCNQ2- and KCNQ3-associated benign familial epilepsy syndromes.Annals of the Child Neurology Society · 2023Review
- Frontline Sodium Channel-Blocking Antiseizure Medicine Use Promotes Future Onset of Drug-Resistant Chronic Seizures.International journal of molecular sciences · 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
- Neonatal Scn1b-null mice have sinoatrial node dysfunction, altered atrial structure, and atrial fibrillation.JCI insight · 2022Article
- S-acylation-dependent membrane microdomain localization of the regulatory Kvβ2.1 subunit.Cellular and molecular life sciences : CMLS · 2022Article
- Ventricular voltage-gated ion channels: Detection, characteristics, mechanisms, and drug safety evaluation.Clinical and translational medicine · 2021Review
- Sodium channel β1 subunits participate in regulated intramembrane proteolysis-excitation coupling.JCI insight · 2021Article
- Voltage Gated Sodium Channel Genes in Epilepsy: Mutations, Functional Studies, and Treatment Dimensions.Frontiers in neurology · 2021Review
- Sexually Divergent Mortality and Partial Phenotypic Rescue After Gene Therapy in a Mouse Model of Dravet Syndrome.Human gene therapy · 2020Article
- The Role of Kv7.2 in Neurodevelopment: Insights and Gaps in Our Understanding.Frontiers in physiology · 2020Review
- SCN1B-linked early infantile developmental and epileptic encephalopathy.Annals of clinical and translational neurology · 2019Article
- Exploring the molecular basis of neuronal excitability in a vocal learner.BMC genomics · 2019Article
- Identification of rare variants in cardiac sodium channel β4-subunit gene SCN4B associated with ventricular tachycardia.Molecular genetics and genomics : MGG · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Voltage-gated sodium (Na(V)) and potassium (K(V)) channels are critical components of neuronal action potential generation and propagation. Here, we report that Na(V)β1 encoded by SCN1b, an integral subunit of Na(V) channels, coassembles with and modulates the biophysical properties of K(V)1 and K(V)7 channels, but not K(V)3 channels, in an isoform-specific manner. Distinct domains of Na(V)β1 are involved in modulation of the different K(V) channels. Studies with channel chimeras demonstrate that Na(V)β1-mediated changes in activation kinetics and voltage dependence of activation require interaction of Na(V)β1 with the channel's voltage-sensing domain, whereas changes in inactivation and deactivation require interaction with the channel's pore domain. A molecular model based on docking studies shows Na(V)β1 lying in the crevice between the voltage-sensing and pore domains of K(V) channels, making significant contacts with the S1 and S5 segments. Cross-modulation of Na(V) and K(V) channels by Na(V)β1 may promote diversity and flexibility in the overall control of cellular excitability and signaling.
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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.