ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
AKAP79/150 signal complexes in G-protein modulation of neuronal ion channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 57 citations in OpenAlex.
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- Pharmacological Activation of Neuronal Voltage-Gated Kv7/KCNQ/M-Channels for Potential Therapy of Epilepsy and Pain.Handbook of experimental pharmacology · 2021Article
- Control of Neuronal Excitability by Cell Surface Receptor Density and Phosphoinositide Metabolism.Frontiers in pharmacology · 2021Article
- Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021Article
- Vascular Kv7 channels control intracellular CaCell calcium · 2020Article
- Article
- AKAP5 complex facilitates purinergic modulation of vascular L-type CaNature communications · 2020Article
- Heteromeric Channels Formed From Alternating Kv7.4 and Kv7.5 α-Subunits Display Biophysical, Regulatory, and Pharmacological Characteristics of Smooth Muscle M-Currents.Frontiers in physiology · 2020Article
- A GeLife · 2019Article
- Gq-Coupled Muscarinic Receptor Enhancement of KCNQ2/3 Channels and Activation of TRPC Channels in Multimodal Control of Excitability in Dentate Gyrus Granule Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- A-Kinase-Anchoring Protein (AKAP150) is expressed in Astrocytes and Upregulated in Response to Ischemia.Neuroscience · 2018Article
- M-type KBritish journal of pharmacology · 2018Review
- Potential for therapeutic targeting of AKAP signaling complexes in nervous system disorders.Pharmacology & therapeutics · 2018Review
- Ser1928 phosphorylation by PKA stimulates the L-type Ca2+ channel CaV1.2 and vasoconstriction during acute hyperglycemia and diabetes.Science signaling · 2017Article
- Kv7 Channel Activation Underpins EPAC-Dependent Relaxations of Rat Arteries.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Article
- Membrane coordination of receptors and channels mediating the inhibition of neuronal ion currents by ADP.Purinergic signalling · 2016Article
- Drosophila SLC5A11 Mediates Hunger by Regulating K(+) Channel Activity.Current biology : CB · 2016Article
- Localised intracellular signalling in neurons.The Journal of physiology · 2016Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Voltage-gated M-type (KCNQ) K+ channels play critical roles in regulation of neuronal excitability. Previous work showed A-kinase-anchoring protein (AKAP)79/150-mediated protein kinase C (PKC) phosphorylation of M channels to be involved in M current (I(M)) suppression by muscarinic M1, but not bradykinin B2, receptors. In this study, we first explored whether purinergic and angiotensin suppression of I(M) in superior cervical ganglion (SCG) sympathetic neurons involves AKAP79/150. Transfection into rat SCG neurons of ΔA-AKAP79, which lacks the A domain necessary for PKC binding, or the absence of AKAP150 in AKAP150(-/-) mice, did not affect I(M) suppression by purinergic agonist or by bradykinin, but reduced I(M) suppression by muscarinic agonist and angiotensin II. Transfection of AKAP79, but not ΔA-AKAP79 or AKAP15, rescued suppression of I(M) by muscarinic receptors in AKAP150(-/-) neurons. We also tested association of AKAP79 with M(1), B(2), P2Y(6), and AT(1) receptors, and KCNQ2 and KCNQ3 channels, via Förster resonance energy transfer (FRET) on Chinese hamster ovary cells under total internal refection fluorescence microscopy, which revealed substantial FRET between AKAP79 and M1 or AT1 receptors, and with the channels, but only weak FRET with P2Y(6) or B2 receptors. The involvement of AKAP79/150 in G(q/11)-coupled muscarinic regulation of N- and L-type Ca2+) channels and by cAMP/protein kinase A was also studied. We found AKAP79/150 to not play a role in the former, but to be necessary for forskolin-induced upregulation of L-current. Thus, AKAP79/150 action correlates with the PIP(2) (phosphatidylinositol 4,5-bisphosphate)-depletion mode of I(M) suppression, but does not generalize to G(q/11)-mediated inhibition of N- or L-type Ca2+ channels.
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