ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated protein kinase increases current density in dorsal root ganglion neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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106 citing papers in PubMed, 173 citations in OpenAlex.
- Botulinum toxin type A attenuates trigeminal neuralgia-like pain by suppressing CGRP release and modulating NaV1.7-associated signaling.The journal of headache and pain · 2026Article
- Structure and function of voltage-gated sodium channel Nav1.6: Involvement in the pathological process of neural injury.Neural regeneration research · 2026Article
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- The Excelsatoxin A-Receptor TMEM233 Modulates Nav1.8.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Microbial PAMPs-PRR driven neuroimmune signaling in the development of post-infectious persistent pain.Anesthesiology and perioperative science · 2026Review
- Incision-triggered neuroimmune remodeling of nociceptor ion channels: from postoperative inflammation to pain chronification.Frontiers in immunology · 2026Review
- Epidermal growth factor receptor signaling modulates postoperative pain and inflammatory responses.Frontiers in immunology · 2026Review
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- Targeting sodium channels - challenges for acute pain and the leap to chronic pain.Nature reviews. Neurology · 2025Review
- Inhibition of the GSK3β/Nav1.6 complex suppresses early-stage Alzheimer's hyperexcitability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Inhibiting Nav1.8 for pain: Lessons from patients and from neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Neuronal p38 MAPK Signaling Contributes to Cisplatin-Induced Peripheral Neuropathy.Antioxidants (Basel, Switzerland) · 2025Article
- Spinal neuron-glial crosstalk and ion channel dysregulation in diabetic neuropathic pain.Frontiers in immunology · 2025Review
- Critical Role of p38α MAPK Subclass in the Development of Pain Hypersensitivity After Hind Paw Incision.Journal of pain research · 2025Article
- Regulation of voltage-gated sodium channels by TNF-α during herpes simplex virus latency establishment.Journal of neurovirology · 2024Article
- Chemokine CXCL13-CXCR5 signaling in neuroinflammation and pathogenesis of chronic pain and neurological diseases.Cellular & molecular biology letters · 2024Review
- Sustained nerve growth factor-induced C-nociceptor sensitization to electrical sinusoidal stimulation in humans.Pain reports · 2024Article
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- Disordered but effective: short linear motifs as gene therapy targets for hyperexcitability disorders.The Journal of clinical investigation · 2024Article
46 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sensory neuron-specific sodium channel Na(v)1.8 and p38 mitogen-activated protein kinase are potential therapeutic targets within nociceptive dorsal root ganglion (DRG) neurons in inflammatory, and possibly neuropathic, pain. Na(v)1.8 channels within nociceptive DRG neurons contribute most of the inward current underlying the depolarizing phase of action potentials. Nerve injury and inflammation of peripheral tissues cause p38 activation in DRG neurons, a process that may contribute to nociceptive neuron hyperexcitability, which is associated with pain. However, how substrates of activated p38 contribute to DRG neuron hyperexcitability is currently not well understood. We report here, for the first time, that Na(v)1.8 and p38 are colocalized in DRG neurons, that Na(v)1.8 within DRG neurons is a substrate for p38, and that direct phosphorylation of the Na(v)1.8 channel by p38 regulates its function in these neurons. We show that direct phosphorylation of Na(v)1.8 at two p38 phospho-acceptor serine residues on the L1 loop (S551 and S556) causes an increase in Na(v)1.8 current density that is not accompanied by changes in gating properties of the channel. Our study suggests a mechanism by which activated p38 contributes to inflammatory, and possibly neuropathic, pain through a p38-mediated increase of Na(v)1.8 current density.
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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.