ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Three mechanisms underlie KCNQ2/3 heteromeric potassium M-channel potentiation.
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 53 papers.
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53 citing papers in PubMed, 78 citations in OpenAlex.
- Molecular Basis for Activation to Inhibition Switching in Kv7.2 Channel Modulators.Angewandte Chemie (International ed. in English) · 2026Article
- Discovery of Novel Bicyclic Pyrazole Amides as Potent Neuronal KACS medicinal chemistry letters · 2026Article
- Temporal multi-omic exploration of the ventral tegmental area in chronic pain and passive coping behaviors.iScience · 2026Article
- 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
- Discovery of a potent, Kv7.3-selective potassium channel opener from a Polynesian traditional botanical anticonvulsant.Communications chemistry · 2024Article
- Effect of a sensing charge mutation on the deactivation of KV7.2 channels.The Journal of general physiology · 2024Article
- Phox2b-expressing neurons contribute to breathing problems in Kcnq2 loss- and gain-of-function encephalopathy models.Nature communications · 2023Article
- Ancient medicinal plant rosemary contains a highly efficacious and isoform-selective KCNQ potassium channel opener.Communications biology · 2023Article
- Site and Mechanism of ML252 Inhibition of Kv7 Voltage-Gated Potassium Channels.Function (Oxford, England) · 2023Article
- Electro-mechanical coupling of KCNQ channels is a target of epilepsy-associated mutations and retigabine.Science advances · 2022Article
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension.Cardiovascular research · 2022Article
- PIPCommunications biology · 2021Article
- The Amyloid Precursor Protein C99 Fragment Modulates Voltage-Gated Potassium Channels.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Article
- CRISPR knockdown of Kcnq3 attenuates the M-current and increases excitability of NPY/AgRP neurons to alter energy balance.Molecular metabolism · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Familial neonatal seizures caused by the Kv7.3 selectivity filter mutation T313I.Epilepsia open · 2020Article
- SMIT (Sodium-Myo-Inositol Transporter) 1 Regulates Arterial Contractility Through the Modulation of Vascular Kv7 Channels.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- The ubiquitous flavonoid quercetin is an atypical KCNQ potassium channel activator.Communications biology · 2020Article
- The Epilepsy of Infancy With Migrating Focal Seizures: Identification ofFrontiers in cellular neuroscience · 2020Article
- KCNQ5 activation is a unifying molecular mechanism shared by genetically and culturally diverse botanical hypotensive folk medicines.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The non-inactivating potassium M-current exerts a strong influence on neuronal excitability. The channels responsible for this current are made up of KCNQ subunits, and mutations in most of these produce human pathologies. Notably, in terms of excitation, mutations in either KCNQ2 or KCNQ3 lead to benign neonatal familial convulsions. Although a mere reduction of 25% in KCNQ2/3 function can increase excitability to epileptogenic levels, the potentiation of these subunits has anti-epileptogenic effects. After KCNQ2/3 heteromerization, current levels can augment as much as 10-fold, and we have discovered that there are three processes underlying this potentiation. First, there is an increase in the number of channels inserted in the membrane after heteromerization of the C-terminal region. Second, the N-terminal domain from KCNQ2 exerts a negative influence on the current level. Finally, Ala 315 of KCNQ3, a residue located in the inner vestibule after the selectivity filter, plays a critical role in preventing current flow in KCNQ3 homomeric channels, whereas it is permissive in heteromers in combination with Thr at the equivalent 276 position of KCNQ2.
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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.