ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
KCNQ2 is a nodal K+ channel.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers.
What it found
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The trial behind it
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Who cites it
227 citing papers in PubMed, 439 citations in OpenAlex.
- Cold aggravates abnormal excitability of motor axons in oxaliplatin-treated patients.Muscle & nerve · 2020Trial
- Activation of axonal Kv7 channels in human peripheral nerve by flupirtine but not placebo - therapeutic potential for peripheral neuropathies: results of a randomised controlled trial.Journal of translational medicine · 2013Trial
- Axon Initial Segment: Structure, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Coupling of functionality to trafficking of KCNQ2/3 potassium channels at the axon initial segment.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Distribution of Voltage-Gated Sodium Channels and Scaffolding Proteins on Vestibular Calyx Ending Delineates the Axon Initial Segment.The Journal of comparative neurology · 2026Article
- Loose-patch recordings reveal differential Kv7-dependent effects on spontaneous excitatory activity in control and epileptic CA1.Frontiers in neurology · 2026Article
- TDP-43-dependent mis-splicing of KCNQ2 triggers intrinsic neuronal hyperexcitability in ALS/FTD.Nature neuroscience · 2025Article
- Cytoskeletal scaffolding of NaCurrent opinion in cell biology · 2025Review
- A hierarchy of PDZ domain scaffolding proteins clusters the Kv1 KScience advances · 2025Article
- Axon initial segment structure and function in health and disease.Physiological reviews · 2025Review
- Targeting Kv7 Potassium Channels for Epilepsy.CNS drugs · 2025Review
- Whole exome sequencing revealed ultra-rare genetic variations in juvenile myoclonic epilepsy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Article
- Potassium channel clustering: mechanisms shaping axonal excitability.Frontiers in cellular neuroscience · 2025Review
- An ankyrin G-binding motif mediates TRAAK periodic localization at axon initial segments of hippocampal pyramidal neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Plural molecular and cellular mechanisms of pore domainbioRxiv : the preprint server for biology · 2024Article
- Ion Channel and Transporter Involvement in Chemotherapy-Induced Peripheral Neurotoxicity.International journal of molecular sciences · 2024Review
- Glial KCNQ KNeuron · 2024Article
- Functional myelin in cognition and neurodevelopmental disorders.Cellular and molecular life sciences : CMLS · 2024Review
- rdHSV-CA8 non-opioid analgesic gene therapy decreases somatosensory neuronal excitability by activating Kv7 voltage-gated potassium channels.Frontiers in molecular neuroscience · 2024Article
167 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
Mutations in the gene encoding the K+ channel KCNQ2 cause neonatal epilepsy and myokymia, indicating that KCNQ2 regulates the excitability of CNS neurons and motor axons, respectively. We show here that KCNQ2 channels are functional components of axon initial segments and nodes of Ranvier, colocalizing with ankyrin-G and voltage-dependent Na+ channels throughout the CNS and PNS. Retigabine, which opens KCNQ channels, diminishes axonal excitability. Linopirdine, which blocks KCNQ channels, prolongs the repolarization of the action potential in neonatal nerves. The clustering of KCNQ2 at nodes and initial segments lags that of ankyrin-G during development, and both ankyrin-G and KCNQ2 can be coimmunoprecipitated in the brain. KCNQ3 is also a component of some initial segments and nodes in the brain. The diminished activity of mutant KCNQ2 channels accounts for neonatal epilepsy and myokymia; the cellular locus of these effects may be axonal initial segments and nodes.
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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.