ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Voltage-gated Na+ channel β1B: a secreted cell adhesion molecule involved in human epilepsy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 101 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
- New focus on cardiac voltage-gated sodium channel β1 and β1B: Novel targets for treating and understanding arrhythmias?Heart rhythm · 2025Review
- Decreased ability to manage increases in reactive oxygen species may underlie susceptibility to arrhythmias in mice lackingAmerican journal of physiology. Heart and circulatory physiology · 2024Article
- Development and characterization of the mode-of-action of inhibitory and agonist peptides targeting the voltage-gated sodium channel SCN1B beta-subunit.Journal of molecular and cellular cardiology · 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
- SCN1B Genetic Variants: A Review of the Spectrum of Clinical Phenotypes and a Report of Early Myoclonic Encephalopathy.Children (Basel, Switzerland) · 2022Review
- Chemical and Biological Tools for the Study of Voltage-Gated Sodium Channels in Electrogenesis and Nociception.Chembiochem : a European journal of chemical biology · 2022Review
- Neonatal Scn1b-null mice have sinoatrial node dysfunction, altered atrial structure, and atrial fibrillation.JCI insight · 2022Article
- Structural Advances in Voltage-Gated Sodium Channels.Frontiers in pharmacology · 2022Review
- Article
- Modulation of the effects of class Ib antiarrhythmics on cardiac NaV1.5-encoded channels by accessory NaVβ subunits.JCI insight · 2021Article
- Sodium channel β1 subunits participate in regulated intramembrane proteolysis-excitation coupling.JCI insight · 2021Article
- Comprehensive Analysis of Genes Associated With Sudden Infant Death Syndrome.Frontiers in pediatrics · 2021Article
- Molecular Pathology of Sodium Channel Beta-Subunit Variants.Frontiers in pharmacology · 2021Article
- Voltage Gated Sodium Channel Genes in Epilepsy: Mutations, Functional Studies, and Treatment Dimensions.Frontiers in neurology · 2021Review
- Sodium channel β1 subunits are post-translationally modified by tyrosine phosphorylation,The Journal of biological chemistry · 2020Article
- The Sodium Channel B4-Subunits are Dysregulated in Temporal Lobe Epilepsy Drug-Resistant Patients.International journal of molecular sciences · 2020Article
- AnFrontiers in cell and developmental biology · 2020Article
- Inhibitory Effect of Eslicarbazepine Acetate and S-Licarbazepine on NaFrontiers in pharmacology · 2020Article
- Computational Investigation of Voltage-Gated Sodium Channel β3 Subunit Dynamics.Frontiers in molecular biosciences · 2020Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Scn1b-null mice have a severe neurological and cardiac phenotype. Human mutations in SCN1B result in epilepsy and cardiac arrhythmia. SCN1B is expressed as two developmentally regulated splice variants, β1 and β1B, that are each expressed in brain and heart in rodents and humans. Here, we studied the structure and function of β1B and investigated a novel human SCN1B epilepsy-related mutation (p.G257R) unique to β1B. We show that wild-type β1B is not a transmembrane protein, but a soluble protein expressed predominantly during embryonic development that promotes neurite outgrowth. Association of β1B with voltage-gated Na+ channels Na(v)1.1 or Na(v)1.3 is not detectable by immunoprecipitation and β1B does not affect Na(v)1.3 cell surface expression as measured by [(3)H]saxitoxin binding. However, β1B coexpression results in subtle alteration of Na(v)1.3 currents in transfected cells, suggesting that β1B may modulate Na+ current in brain. Similar to the previously characterized p.R125C mutation, p.G257R results in intracellular retention of β1B, generating a functional null allele. In contrast, two other SCN1B mutations associated with epilepsy, p.C121W and p.R85H, are expressed at the cell surface. We propose that β1B p.G257R may contribute to epilepsy through a mechanism that includes intracellular retention resulting in aberrant neuronal pathfinding.
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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.