ArticleThe Journal of biological chemistry2010
The sodium channel {beta}3-subunit induces multiphasic gating in NaV1.3 and affects fast inactivation via distinct intracellular regions.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 38 citations in OpenAlex.
- Isoform-specific N-linked glycosylation of NaV channel α-subunits alters β-subunit binding sites.The Journal of general physiology · 2025Article
- The β3-subunit modulates the effect of venom peptides ProTx-II and OD1 on NaJournal of cellular physiology · 2023Article
- Structure and Function of Sodium Channel Nav1.3 in Neurological Disorders.Cellular and molecular neurobiology · 2023Review
- Loss of function of OTUD7A in the schizophrenia- associated 15q13.3 deletion impairs synapse development and function in human neurons.American journal of human genetics · 2022Article
- iPSCs and DRGs: stepping stones to new pain therapies.Trends in molecular medicine · 2022Review
- Pharmacological Dissection of the Crosstalk between NaInternational journal of molecular sciences · 2022Article
- A novel gain-of-function sodium channel β2 subunit mutation in idiopathic small fiber neuropathy.Journal of neurophysiology · 2021Article
- Supramolecular clustering of the cardiac sodium channel Nav1.5 in HEK293F cells, with and without the auxiliary β3-subunit.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Gating control of the cardiac sodium channel Nav1.5 by its β3-subunit involves distinct roles for a transmembrane glutamic acid and the extracellular domain.The Journal of biological chemistry · 2019Article
- Exploring the molecular basis of neuronal excitability in a vocal learner.BMC genomics · 2019Article
- Emerging roles for multifunctional ion channel auxiliary subunits in cancer.Cell calcium · 2019Review
- Transcriptional and epigenomic landscapes of CNS and non-CNS vascular endothelial cells.eLife · 2018Article
- Voltage-gated sodium channel β subunits: The power outside the pore in brain development and disease.Neuropharmacology · 2018Review
- Multiple targets for flecainide action: implications for cardiac arrhythmogenesis.British journal of pharmacology · 2018Review
- Mutations in SCN3A cause early infantile epileptic encephalopathy.Annals of neurology · 2018Article
- A single Markov-type kinetic model accounting for the macroscopic currents of all human voltage-gated sodium channel isoforms.PLoS computational biology · 2017Article
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
- Novel SCN9A mutations underlying extreme pain phenotypes: unexpected electrophysiological and clinical phenotype correlations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Synergetic action of domain II and IV underlies persistent current generation in Nav1.3 as revealed by a tarantula toxin.Scientific reports · 2015Article
- A new look at sodium channel β subunits.Open biology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Electrical excitability in neurons depends on the activity of membrane-bound voltage gated sodium channels (Na(v)) that are assembled from an ion conducting α-subunit and often auxiliary β-subunits. The α-subunit isoform Na(v)1.3 occurs in peripheral neurons together with the Na(v) β3-subunit, both of which are coordinately up-regulated in rat dorsal root ganglion neurons after nerve injury. Here we examine the effect of the β3-subunit on the gating behavior of Na(v)1.3 using whole cell patch clamp electrophysiology in HEK-293 cells. We show that β3 depolarizes the voltage sensitivity of Na(v)1.3 activation and inactivation and induces biphasic components of the inactivation curve. We detect both a fast and a novel slower component of inactivation, and we show that the β3-subunit increases the fraction of channels inactivating by the slower component. Using CD and NMR spectroscopy, we report the first structural analysis of the intracellular domain of any Na(v) β-subunit. We infer the presence of a region within the β3-subunit intracellular domain that has a propensity to form a short amphipathic α-helix followed by a structurally disordered sequence, and we demonstrate a role for both of these regions in the selective stabilization of fast inactivation. The complex gating behavior induced by β3 may contribute to the known hyperexcitability of peripheral neurons under those physiological conditions where expression of β3 and Na(v)1.3 are both enhanced.
Indexed as
Identifiers
What OpenQuestion holds
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.