ArticleThe Journal of biological chemistry2012
Interaction of voltage-gated sodium channel Nav1.6 (SCN8A) with microtubule-associated protein Map1b.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- MAP1B Variants Disrupt Neuronal Migration: Insights From Three Novel Families.Clinical genetics · 2026Article
- Sculpting excitable membranes: voltage-gated ion channel delivery and distribution.Nature reviews. Neuroscience · 2025Review
- Nociceptor sodium channels shape subthreshold phase, upstroke, and shoulder of action potentials.The Journal of general physiology · 2025Article
- Tau isoform-specific enhancement of L-type calcium current and augmentation of afterhyperpolarization in rat hippocampal neurons.Scientific reports · 2022Article
- A multi-omic analysis of the dorsal striatum in an animal model of divergent genetic risk for alcohol use disorder.Journal of neurochemistry · 2021Article
- Sodium channelopathies in neurodevelopmental disorders.Nature reviews. Neuroscience · 2021Review
- Trafficking mechanisms underlying NaChannels (Austin, Tex.) · 2020Review
- Epilepsy-Related Voltage-Gated Sodium Channelopathies: A Review.Frontiers in pharmacology · 2020Review
- Immortalized Dorsal Root Ganglion Neuron Cell Lines.Frontiers in cellular neuroscience · 2020Review
- Case studies in neuroscience: a novel amino acid duplication in the NHJournal of neurophysiology · 2019Article
- The MAP1B Binding Domain of NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- PRRT2 controls neuronal excitability by negatively modulating Na+ channel 1.2/1.6 activity.Brain : a journal of neurology · 2018Article
- PiT2 regulates neuronal outgrowth through interaction with microtubule-associated protein 1B.Scientific reports · 2017Article
- MAP1B Light Chain Modulates Synaptic Transmission via AMPA Receptor Intracellular Trapping.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Single amino acid deletion in transmembrane segment D4S6 of sodium channel Scn8a (Nav1.6) in a mouse mutant with a chronic movement disorder.Neurobiology of disease · 2016Article
- Pathogenic mechanism of recurrent mutations of SCN8A in epileptic encephalopathy.Annals of clinical and translational neurology · 2016Article
- Amyloid precursor protein enhances Nav1.6 sodium channel cell surface expression.The Journal of biological chemistry · 2015Article
- De novo gain-of-function and loss-of-function mutations of SCN8A in patients with intellectual disabilities and epilepsy.Journal of medical genetics · 2015Article
- Convulsive seizures and SUDEP in a mouse model of SCN8A epileptic encephalopathy.Human molecular genetics · 2015Article
- CaV2.2 channel cell surface expression is regulated by the light chain 1 (LC1) of the microtubule-associated protein B (MAP1B) via UBE2L3-mediated ubiquitination and degradation.Pflugers Archiv : European journal of physiology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanism by which voltage-gated sodium channels are trafficked to the surface of neurons is not well understood. Our previous work implicated the cytoplasmic N terminus of the sodium channel Na(v)1.6 in this process. We report that the N terminus plus the first transmembrane segment (residues 1-153) is sufficient to direct a reporter to the cell surface. To identify proteins that interact with the 117-residue N-terminal domain, we carried out a yeast two-hybrid screen of a mouse brain cDNA library. Three clones containing overlapping portions of the light chain of microtubule-associated protein Map1b (Mtap1b) were recovered from the screen. Interaction between endogenous Na(v)1.6 channels and Map1b in mouse brain was confirmed by co-immunoprecipitation. Map1b did not interact with the N terminus of the related channel Na(v)1.1. Alanine-scanning mutagenesis of the Na(v)1.6 N terminus demonstrated that residues 77-80 (VAVP) contribute to interaction with Map1b. Co-expression of Na(v)1.6 with Map1b in neuronal cell line ND7/23 resulted in a 50% increase in current density, demonstrating a functional role for this interaction. Mutation of the Map1b binding site of Na(v)1.6 prevented generation of sodium current in transfected cells. The data indicate that Map1b facilitates trafficking of Na(v)1.6 to the neuronal cell surface.
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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.