ReviewNeuropharmacology2018
Voltage-gated sodium channel β subunits: The power outside the pore in brain development and disease.
Review in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed.
- Precision acupuncture for chemotherapy-induced peripheral neuropathy: multitarget mechanisms and integrated clinical translation framework.Frontiers in neurology · 2026Review
- Voltage-Gated Sodium Channel Dysfunction in Epilepsy: Zebrafish Models for Therapeutics.Biomedicines · 2025Review
- Saxitoxin: A Comprehensive Review of Its History, Structure, Toxicology, Biosynthesis, Detection, and Preventive Implications.Marine drugs · 2025Review
- New focus on cardiac voltage-gated sodium channel β1 and β1B: Novel targets for treating and understanding arrhythmias?Heart rhythm · 2025Review
- A novel gain-of-function mutationAmerican journal of cardiovascular disease · 2025Article
- Genetic mechanisms of dynamic functional connectivity density in diabetic retinopathy brains: a combined transcriptomic and resting-state functional magnetic resonance imaging study.Frontiers in cellular neuroscience · 2025Article
- Developmental exposure of zebrafish to saxitoxin causes altered expression of genes associated with axonal growth.Neurotoxicology · 2024Article
- In Silico Screening Identification of Fatty Acids and Fatty Acid Derivatives with Antiseizure Activity: In Vitro and In Vivo Validation.Pharmaceutics · 2024Article
- Short-term plasticity as 'energetic memory' of ion channel components of action potential.Royal Society open science · 2024Article
- Anti-PD-1 treatment protects against seizure by suppressing sodium channel function.CNS neuroscience & therapeutics · 2024Article
- Experimental and computational evidence that Calpain-10 binds to the carboxy terminus of NaScientific reports · 2024Article
- Molecular and functional profiling of cell diversity and identity in the lateral superior olive, an auditory brainstem center with ascending and descending projections.Frontiers in cellular neuroscience · 2024Article
- Association between human blood metabolites and cerebral cortex architecture: evidence from a Mendelian randomization study.Frontiers in neurology · 2024Article
- Clinical and Genetic Features of Dravet Syndrome: A Prime Example of the Role of Precision Medicine in Genetic Epilepsy.International journal of molecular sciences · 2023Review
- 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
- Defects in early synaptic formation and neuronal function in Prader-Willi syndrome.Scientific reports · 2023Article
- Heterogeneity of voltage gated sodium current density between neurons decorrelates spiking and suppresses network synchronization in Scn1b null mouse models.Scientific reports · 2023Article
- Glycans and Carbohydrate-Binding/Transforming Proteins in Axon Physiology.Advances in neurobiology · 2023Article
- SCN1B Genetic Variants: A Review of the Spectrum of Clinical Phenotypes and a Report of Early Myoclonic Encephalopathy.Children (Basel, Switzerland) · 2022Review
- Therapeutic Potential of Targeting Regulated Intramembrane Proteolysis Mechanisms of Voltage-Gated Ion Channel Subunits and Cell Adhesion Molecules.Pharmacological reviews · 2022Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Voltage gated sodium channels (VGSCs) were first identified in terms of their role in the upstroke of the action potential. The underlying proteins were later identified as saxitoxin and scorpion toxin receptors consisting of α and β subunits. We now know that VGSCs are heterotrimeric complexes consisting of a single pore forming α subunit joined by two β subunits; a noncovalently linked β1 or β3 and a covalently linked β2 or β4 subunit. VGSC α subunits contain all the machinery necessary for channel cell surface expression, ion conduction, voltage sensing, gating, and inactivation, in one central, polytopic, transmembrane protein. VGSC β subunits are more than simple accessories to α subunits. In the more than two decades since the original cloning of β1, our knowledge of their roles in physiology and pathophysiology has expanded immensely. VGSC β subunits are multifunctional. They confer unique gating mechanisms, regulate cellular excitability, affect brain development, confer distinct channel pharmacology, and have functions that are independent of the α subunits. The vast array of functions of these proteins stems from their special station in the channelome: being the only known constituents that are cell adhesion and intra/extracellular signaling molecules in addition to being part of channel complexes. This functional trifecta and how it goes awry demonstrates the power outside the pore in ion channel signaling complexes, broadening the term channelopathy beyond defects in ion conduction. This article is part of the Special Issue entitled 'Channelopathies.'
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