ArticleNature neuroscience2003
AKAP150 signaling complex promotes suppression of the M-current by muscarinic agonists.
Article in Nature neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
What it found
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Who cites it
132 citing papers in PubMed, 238 citations in OpenAlex.
- Physiological 17β-oestradiol inhibits KChannels (Austin, Tex.) · 2026Article
- Therapeutic potential of small molecules that block receptor-induced Kv7/M-current suppression in neuroprotection, seizures, and pain.British journal of pharmacology · 2026Article
- Activation of Dopamine D1 Receptors at the Axon Initial Segment-Like Process of Retinal AII Amacrine Cells Modulates Action Potential Firing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- A case of early epileptic encephalopathy caused by new mutation at W218C inBiochemistry and biophysics reports · 2025Article
- Review
- AKAP150-anchored PKA regulates synaptic transmission and plasticity, neuronal excitability and CRF neuromodulation in the mouse lateral habenula.Communications biology · 2024Article
- Exploring AKAPs in visual signaling.Frontiers in molecular neuroscience · 2024Review
- Dehydroepiandrosterone Sulfate (DHEAS) Is an Endogenous Kv7 Channel Modulator That Reduces Kv7/M-Current Suppression and Inflammatory Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Involvement of CaCellular and molecular neurobiology · 2023Article
- A journey from molecule to physiology andFrontiers in pharmacology · 2023Review
- Antagonism of the Muscarinic Acetylcholine Type 1 Receptor Enhances Mitochondrial Membrane Potential and Expression of Respiratory Chain Components via AMPK in Human Neuroblastoma SH-SY5Y Cells and Primary Neurons.Molecular neurobiology · 2022Article
- HumanJournal of neurophysiology · 2022Article
- Roles of Key Ion Channels and Transport Proteins in Age-Related Hearing Loss.International journal of molecular sciences · 2021Review
- Neuropeptide S Receptor Stimulation Excites Principal Neurons in Murine Basolateral Amygdala through a Calcium-Dependent Decrease in Membrane Potassium Conductance.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021Review
- Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021Article
- Pharmacological Activation of Neuronal Voltage-Gated Kv7/KCNQ/M-Channels for Potential Therapy of Epilepsy and Pain.Handbook of experimental pharmacology · 2021Article
- Vascular Kv7 channels control intracellular CaCell calcium · 2020Article
- AKAP Signaling Islands: Venues for Precision Pharmacology.Trends in pharmacological sciences · 2020Review
- Article
72 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
M-type (KCNQ2/3) potassium channels are suppressed by activation of G(q/11)-coupled receptors, thereby increasing neuronal excitability. We show here that rat KCNQ2 can bind directly to the multivalent A-kinase-anchoring protein AKAP150. Peptides that block AKAP150 binding to the KCNQ2 channel complex antagonize the muscarinic inhibition of the currents. A mutant form of AKAP150, AKAP(DeltaA), which is unable to bind protein kinase C (PKC), also attenuates the agonist-induced current suppression. Analysis of recombinant KCNQ2 channels suggests that targeting of PKC through association with AKAP150 is important for the inhibition. Phosphorylation of KCNQ2 channels was increased by muscarinic stimulation; this was prevented either by coexpression with AKAP(DeltaA) or pretreatment with PKC inhibitors that compete with diacylglycerol. These inhibitors also reduced muscarinic inhibition of M-current. Our data indicate that AKAP150-bound PKC participates in receptor-induced inhibition of the M-current.
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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.