ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
KIF5B promotes the forward transport and axonal function of the voltage-gated sodium channel Nav1.8.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- Infantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese Families.PloS one · 2016Trial
- Mitocytosis, mitophagy, and apoptosis coordinately drive mitochondrial clearance to regulate myogenic differentiation.Journal of advanced research · 2026Article
- Microtubule Cytoskeleton Dysfunction in Chronic Pain: Mechanisms of Transport Failure and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- Article
- Sculpting excitable membranes: voltage-gated ion channel delivery and distribution.Nature reviews. Neuroscience · 2025Review
- Real-time imaging of axonal membrane protein life cycles.Nature protocols · 2024Review
- A Novel Ubiquitin Ligase Adaptor PTPRN Suppresses Seizure Susceptibility through Endocytosis of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Endophilin A2 controls touch and mechanical allodynia via kinesin-mediated Piezo2 trafficking.Military Medical Research · 2024Article
- Ropivacaine Promotes Axon Regeneration by Regulating Nav1.8-mediated Macrophage Signaling after Sciatic Nerve Injury in Rats.Anesthesiology · 2023Article
- Microtubule plus-end tracking proteins: novel modulators of cardiac sodium channels and arrhythmogenesis.Cardiovascular research · 2023Article
- Multiple Copies of microRNA Binding Sites in Long 3'UTR Variants Regulate Axonal Translation.Cells · 2023Article
- Inhibitions and Down-Regulation of Motor Protein Eg5 Expression in Primary Sensory Neurons Reveal a Novel Therapeutic Target for Pathological Pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Study of Anti-Inflammatory and Analgesic Activity of Scorpion Toxins DKK-SP1/2 from ScorpionToxins · 2021Article
- E44Q mutation in NaHeliyon · 2021Article
- Spatiotemporal patterns of gene expression around implanted silicon electrode arrays.Journal of neural engineering · 2021Article
- Astrocyte-derived extracellular vesicles enhance the survival and electrophysiological function of human cortical neurons in vitro.Biomaterials · 2021Article
- ATF4 selectively regulates heat nociception and contributes to kinesin-mediated TRPM3 trafficking.Nature communications · 2021Article
- Structural basis of GABARAP-mediated GABANature communications · 2021Article
- Trafficking mechanisms underlying NaChannels (Austin, Tex.) · 2020Review
- Molecular characterization and distribution of the voltage-gated sodium channel, Para, in the brain of the grasshopper and vinegar fly.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2020Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nav1.8 is a tetrodotoxin-resistant voltage-gated sodium channel selectively expressed in primary sensory neurons. Peripheral inflammation and nerve injury induce Nav1.8 accumulation in peripheral nerves. However, the mechanisms and related significance of channel accumulation in nerves remains unclear. Here we report that KIF5B promotes the forward transport of Nav1.8 to the plasma membrane and axons in dorsal root ganglion (DRG) neurons of the rat. In peripheral inflammation induced through the intraplantar injection of complete Freund's adjuvant, increased KIF5 and Nav1.8 accumulation were observed in the sciatic nerve. The knock-down of KIF5B, a highly expressed member of the KIF5 family in DRGs, reduced the current density of Nav1.8 in both cultured DRG neurons and ND7-23 cells. Overexpression of KIF5B in ND7-23 cells increased the current density and surface expression of Nav1.8, which were abolished through brefeldin A treatment, whereas the increases were lost in KIF5B mutants defective in ATP hydrolysis or cargo binding. Overexpression of KIF5B also decreased the proteasome-associated degradation of Nav1.8. In addition, coimmunoprecipitation experiments showed interactions between the N terminus of Nav1.8 and the 511-620 aa sequence in the stalk domain of KIF5B. Furthermore, KIF5B increased Nav1.8 accumulation, Nav1.8 current, and neuronal excitability detected in the axons of cultured DRG neurons, which were completely abolished by the disruption of interactions between KIF5B and the N terminus of Nav1.8. Therefore, our results reveal that KIF5B is required for the forward transport and axonal function of Nav1.8, suggesting a mechanism for axonal accumulation of Nav1.8 in inflammatory pain.
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