ArticleScientific reports2016
Sodium channel slow inactivation interferes with open channel block.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Specific Binding Agents for the Molecular Recognition of Biotoxins: Recent Advances and Applications in Forensic Toxicology.Molecules (Basel, Switzerland) · 2026Review
- Effects of open-channel blocking peptides in NaBiophysical journal · 2025Article
- Ramped kilohertz-frequency signals produce nerve conduction block without onset response.Journal of neural engineering · 2025Article
- Reverse-engineered models reveal differential membrane properties of autonomic and cutaneous unmyelinated fibers.PLoS computational biology · 2024Article
- The road to evolution of ProTx2: how to be a subtype-specific inhibition of human NaFrontiers in pharmacology · 2024Article
- Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents.The Journal of general physiology · 2023Article
- PI(4,5)P2 regulates the gating of NaV1.4 channels.The Journal of general physiology · 2023Article
- NaExperimental neurology · 2023Article
- Article
- Contributions of NaScientific reports · 2021Article
- Assessing the impact of pain-linked Nav1.7 variants: An example of two variants with no biophysical effect.Channels (Austin, Tex.) · 2021Article
- Cannabidiol inhibits the skeletal muscle Nav1.4 by blocking its pore and by altering membrane elasticity.The Journal of general physiology · 2021Article
- Uncoupling sodium channel dimers restores the phenotype of a pain-linked NaBritish journal of pharmacology · 2020Article
- Effects of Deltamethrin Acute Exposure on Nav1.6 Channels and Medium Spiny Neurons of the Nucleus Accumbens.Toxicology · 2020Article
- Noncanonical Ion Channel Behaviour in Pain.International journal of molecular sciences · 2019Review
- Article
- [Neuropathic pain syndromes and channelopathies].Der Internist · 2019Review
- Pain relief in a neuropathy patient by lacosamide: Proof of principle of clinical translation from patient-specific iPS cell-derived nociceptors.EBioMedicine · 2019Article
- Heat-resistant action potentials require TTX-resistant sodium channels NaThe Journal of general physiology · 2018Article
- Conservation of alternative splicing in sodium channels reveals evolutionary focus on release from inactivation and structural insights into gating.The Journal of physiology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the voltage-gated sodium channel Nav1.7 are linked to inherited pain syndromes such as erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD). PEPD mutations impair Nav1.7 fast inactivation and increase persistent currents. PEPD mutations also increase resurgent currents, which involve the voltage-dependent release of an open channel blocker. In contrast, IEM mutations, whenever tested, leave resurgent currents unchanged. Accordingly, the IEM deletion mutation L955 (ΔL955) fails to produce resurgent currents despite enhanced persistent currents, which have hitherto been considered a prerequisite for resurgent currents. Additionally, ΔL955 exhibits a prominent enhancement of slow inactivation (SI). We introduced mutations into Nav1.7 and Nav1.6 that either enhance or impair SI in order to investigate their effects on resurgent currents. Our results show that enhanced SI is accompanied by impaired resurgent currents, which suggests that SI may interfere with open-channel block.
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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.