Regulation of KCNQ2/KCNQ3 current by G protein cycling (Suh et al 2004)


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Accession:55273
Receptor-mediated modulation of KCNQ channels regulates neuronal excitability. This study concerns the kinetics and mechanism of M1 muscarinic receptor-mediated regulation of the cloned neuronal M channel, KCNQ2/KCNQ3 (Kv7.2/Kv7.3). ... observations were successfully described by a kinetic model representing biochemical steps of the signaling cascade using published rate constants where available. The model supports the following sequence of events for this Gq-coupled signaling: A classical G-protein cycle, including competition for nucleotide-free G-protein by all nucleotide forms and an activation step requiring Mg2, followed by G-protein-stimulated phospholipase C and hydrolysis of PIP2, and finally PIP2 dissociation from binding sites for inositol lipid on the channels so that KCNQ current was suppressed. See paper for details and more.
References:
1 . Suh BC, Horowitz LF, Hirdes W, Mackie K, Hille B (2004) Regulation of KCNQ2-KCNQ3 current by G protein cycling: the kinetics of receptor-mediated signaling by Gq. J Gen Physiol 123:663-83 [PubMed]
2 . Shapiro MS (2004) Why biophysicists make models: quantifying modulation of the M current. J Gen Physiol 123:657-62 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s):
Channel(s): I M;
Gap Junctions:
Receptor(s): Muscarinic; Cholinergic Receptors;
Gene(s):
Transmitter(s):
Simulation Environment: Virtual Cell (web link to model);
Model Concept(s): Ion Channel Kinetics; Signaling pathways; G-protein coupled;
Implementer(s):
Search NeuronDB for information about:  Muscarinic; Cholinergic Receptors; I M;
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