ReviewThe Journal of physiology2008
Regulation of neural KCNQ channels: signalling pathways, structural motifs and functional implications.
Review in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
What it found
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Who cites it
106 citing papers in PubMed, 164 citations in OpenAlex.
- 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
- Physiological 17β-oestradiol inhibits KChannels (Austin, Tex.) · 2026Article
- CRISPR/Cas9-mediatedFrontiers in physiology · 2026Article
- Molecular dynamics of the pathogenic KCNQ2 variant G256W reveal mechanisms of channel dysfunction in epileptic encephalopathy.bioRxiv : the preprint server for biology · 2025Article
- Potassium current inactivation as a novel pathomechanism for KCNQ2 developmental and epileptic encephalopathy.Epilepsia · 2025Article
- Palmitoylation and regulation of potassium-dependent sodium/calcium exchangers (NCKX).Bioscience reports · 2025Article
- Association between Single Nucleotide Polymorphisms ofFoods (Basel, Switzerland) · 2024Article
- G protein βγ regulation of KCNQ-encoded voltage-dependent K channels.Frontiers in physiology · 2024Review
- rdHSV-CA8 non-opioid analgesic gene therapy decreases somatosensory neuronal excitability by activating Kv7 voltage-gated potassium channels.Frontiers in molecular neuroscience · 2024Article
- Functional characterization and in vitro pharmacological rescue of KCNQ2 pore mutations associated with epileptic encephalopathy.Acta pharmacologica Sinica · 2023Article
- Involvement of CaCellular and molecular neurobiology · 2023Article
- Palmitoylation of Voltage-Gated Ion Channels.International journal of molecular sciences · 2022Review
- Evidence for Dual Activation ofInternational journal of molecular sciences · 2022Article
- Neuronal KCNQ2/3 channels are recruited to lipid raft microdomains by palmitoylation of BACE1.The Journal of general physiology · 2022Article
- Functional Characterization of Two Variants at the Intron 6-Exon 7 Boundary of the KCNQ2 Potassium Channel Gene Causing Distinct Epileptic Phenotypes.Frontiers in pharmacology · 2022Article
- Met-Controlled Allosteric Module of Neural Generation as A New Therapeutic Target in Rodent Brain Ischemia.Chinese journal of integrative medicine · 2021Article
- Autism-associated mutations in KProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Roles of Key Ion Channels and Transport Proteins in Age-Related Hearing Loss.International journal of molecular sciences · 2021Review
- Pharmacological Activation of Neuronal Voltage-Gated Kv7/KCNQ/M-Channels for Potential Therapy of Epilepsy and Pain.Handbook of experimental pharmacology · 2021Article
- Alteration of Mesopontine Cholinergic Function by the Lack of KCNQ4 Subunit.Frontiers in cellular neuroscience · 2021Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Neural M-type (KCNQ/Kv7) K(+) channels control somatic excitability, bursting and neurotransmitter release throughout the nervous system. Their activity is regulated by multiple signalling pathways. In superior cervical ganglion sympathetic neurons, muscarinic M(1), angiotensin II AT(1), bradykinin B(2) and purinergic P2Y agonists suppress M current (I(M)). Probes of PLC activity show agonists of all four receptors to induce robust PIP(2) hydrolysis. We have grouped these receptors into two related modes of action. One mode involves depletion of phosphatidylinositol 4,5-bisphosphate (PIP(2)) in the membrane, whose interaction with the channels is thought necessary for their function. The other involves IP(3)-mediated intracellular Ca(2+) signals that stimulate PIP(2) synthesis, preventing its depletion, and suppress I(M) via calmodulin. Carbon-fibre amperometry can evaluate the effect of M channel activity on release of neurotransmitter. Consistent with the dominant role of M current in control of neuronal discharge, M channel openers, or blockers, reduced or augmented the evoked release of noradrenaline neurotransmitter from superior cervical ganglion (SCG) neurons, respectively. We seek to localize the subdomains on the channels critical to their regulation by PIP(2). Based on single-channel recordings from chimeras between high-PIP(2) affinity KCNQ3 and low-PIP(2) affinity KCNQ4 channels, we focus on a 57-residue domain within the carboxy-terminus that is a possible PIP(2) binding site. Homology modelling of this domain using the published structure of IRK1 channels as a template predicts a structure very similar to an analogous region in IRK1 channels, and shows a cluster of basic residues in the KCNQ2 domain to correspond to those implicated in PIP(2) regulation of Kir channels. We discuss some important issues dealing with these topics.
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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.