ArticleProceedings of the National Academy of Sciences of the United States of America2006
Inhibition of a background potassium channel by Gq protein alpha-subunits.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 148 citations in OpenAlex.
- G protein GαThe Journal of biological chemistry · 2026Article
- Transcriptional and functional profiles of muscarinic receptor-expressing neurons in primate lateral prefrontal and anterior cingulate cortices.Communications biology · 2026Article
- PKC isoform-specific targeting of the phosphorylation site SerinePflugers Archiv : European journal of physiology · 2026Article
- Thalamocortical feedback selectively controls pyramidal neuron excitability.Nature communications · 2025Article
- Chronic activation of adrenal Gq signaling induces Cyp11b2 expression in the zona fasciculata and hyperaldosteronism.Molecular and cellular endocrinology · 2024Article
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Gain and loss of TASK3 channel function and its regulation by novel variation cause KCNK9 imprinting syndrome.Genome medicine · 2022Article
- Two-Pore Domain Potassium Channel in Neurological Disorders.The Journal of membrane biology · 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
- Ion Channel Function and Electrical Excitability in the Zona Glomerulosa: A Network Perspective on Aldosterone Regulation.Annual review of physiology · 2021Review
- Comparison of KHandbook of experimental pharmacology · 2021Article
- Lysophosphatidic Acid and Several Neurotransmitters Converge on Rho-Kinase 2 Signaling to Manage Motoneuron Excitability.Frontiers in molecular neuroscience · 2021Article
- The Pharmacology of Two-Pore Domain Potassium Channels.Handbook of experimental pharmacology · 2021Article
- TASK-1 and TASK-3 channels modulate pressure overload-induced cardiac remodeling and dysfunction.American journal of physiology. Heart and circulatory physiology · 2020Article
- Sp1-regulated expression of p11 contributes to motor neuron degeneration by membrane insertion of TASK1.Nature communications · 2019Article
- Molecular Mechanisms of REM Sleep.Frontiers in neuroscience · 2019Review
- Two-pore domain potassium channels: emerging targets for novel analgesic drugs: IUPHAR Review 26.British journal of pharmacology · 2019Review
- Adenosine AThe Journal of physiology · 2018Article
- Muscarinic receptors in adrenal chromaffin cells: physiological role and regulation of ion channels.Pflugers Archiv : European journal of physiology · 2018Review
- Endocytosis: another pathway in receptor-Gq-TASK signalling.The Journal of physiology · 2017Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Two-pore-domain K(+) channels provide neuronal background currents that establish resting membrane potential and input resistance; their modulation provides a prevalent mechanism for regulating cellular excitability. The so-called TASK channel subunits (TASK-1 and TASK-3) are widely expressed, and they are robustly inhibited by receptors that signal through Galphaq family proteins. Here, we manipulated G protein expression and membrane phosphatidylinositol 4,5-bisphosphate (PIP(2)) levels in intact and cell-free systems to provide electrophysiological and biochemical evidence that inhibition of TASK channels by Galphaq-linked receptors proceeds unabated in the absence of phospholipase C (PLC) activity, and instead involves association of activated Galphaq subunits with the channels. Receptor-mediated inhibition of TASK channels was faster and less sensitive to a PLCbeta1-ct minigene construct than inhibition of PIP(2)-sensitive Kir3.4(S143T) homomeric channels that is known to be dependent on PLC. TASK channels were strongly inhibited by constitutively active Galphaq, even by a mutated version that is deficient in PLC activation. Receptor-mediated TASK channel inhibition required exogenous Galphaq expression in fibroblasts derived from Galphaq/11 knockout mice, but proceeded unabated in a cell line in which PIP(2) levels were reduced by regulated overexpression of a lipid phosphatase. Direct application of activated Galphaq, but not other G protein subunits, inhibited TASK channels in excised patches, and constitutively active Galphaq subunits were selectively coimmunoprecipitated with TASK channels. These data indicate that receptor-mediated TASK channel inhibition is independent of PIP(2) depletion, and they suggest a mechanism whereby channel modulation by Galphaq occurs through direct interaction with the ion channel or a closely associated intermediary.
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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.