ArticlePloS one2016
Biophysical and Pharmacological Characterization of Nav1.9 Voltage Dependent Sodium Channels Stably Expressed in HEK-293 Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- A robust expression system reveals distinct gating mechanisms and calmodulin regulation of NaScience advances · 2025Article
- Article
- Nav1.8, an analgesic target for nonpsychotomimetic phytocannabinoids.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Discovery of E0199: A novel compound targeting both peripheral NaJournal of pharmaceutical analysis · 2025Article
- Ion Channel and Transporter Involvement in Chemotherapy-Induced Peripheral Neurotoxicity.International journal of molecular sciences · 2024Review
- The influence of Nav1.9 channels on intestinal hyperpathia and dysmotility.Channels (Austin, Tex.) · 2023Review
- Article
- NaJournal of neurophysiology · 2022Article
- Targeting the tamoxifen receptor within sodium channels to block osteoarthritic pain.Cell reports · 2022Article
- T-Type CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- A-type FHFs mediate resurgent currents through TTX-resistant voltage-gated sodium channels.eLife · 2022Article
- The physiological function of different voltage-gated sodium channels in pain.Nature reviews. Neuroscience · 2021Review
- TRPM4 mediates a subthreshold membrane potential oscillation in respiratory chemoreceptor neurons that drives pacemaker firing and breathing.Cell reports · 2021Article
- Sodium Channel Blockers Modulate Abnormal Activity of Regenerating Nociceptive Corneal Nerves After Surgical Lesion.Investigative ophthalmology & visual science · 2021Article
- Status of peripheral sodium channel blockers for non-addictive pain treatment.Nature reviews. Neurology · 2020Review
- Manipulation of a spider peptide toxin alters its affinity for lipid bilayers and potency and selectivity for voltage-gated sodium channel subtype 1.7.The Journal of biological chemistry · 2020Article
- A 49-residue sequence motif in the C terminus of Nav1.9 regulates trafficking of the channel to the plasma membrane.The Journal of biological chemistry · 2020Article
- Article
- NaV1.6 and NaV1.7 channels are major endogenous voltage-gated sodium channels in ND7/23 cells.PloS one · 2019Article
- Using automated patch clamp electrophysiology platforms in pain-related ion channel research: insights from industry and academia.British journal of pharmacology · 2018Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The voltage dependent sodium channel Nav1.9, is expressed preferentially in peripheral sensory neurons and has been linked to human genetic pain disorders, which makes it target of interest for the development of new pain therapeutics. However, characterization of Nav1.9 pharmacology has been limited due in part to the historical difficulty of functionally expressing recombinant channels. Here we report the successful generation and characterization of human, mouse and rat Nav1.9 stably expressed in human HEK-293 cells. These cells exhibit slowly activating and inactivating inward sodium channel currents that have characteristics of native Nav1.9. Optimal functional expression was achieved by coexpression of Nav1.9 with β1/β2 subunits. While recombinantly expressed Nav1.9 was found to be sensitive to sodium channel inhibitors TC-N 1752 and tetracaine, potency was up to 100-fold less than reported for other Nav channel subtypes despite evidence to support an interaction with the canonical local anesthetic (LA) binding region on Domain 4 S6. Nav1.9 Domain 2 S6 pore domain contains a unique lysine residue (K799) which is predicted to be spatially near the local anesthetic interaction site. Mutation of this residue to the consensus asparagine (K799N) resulted in an increase in potency for tetracaine, but a decrease for TC-N 1752, suggesting that this residue can influence interaction of inhibitors with the Nav1.9 pore. In summary, we have shown that stable functional expression of Nav1.9 in the widely used HEK-293 cells is possible, which opens up opportunities to better understand channel properties and may potentially aid identification of novel Nav1.9 based pharmacotherapies.
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