ArticleBritish journal of pharmacology2007
Identification of a region in the TASK3 two pore domain potassium channel that is critical for its blockade by methanandamide.
Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Two-Pore Domain Potassium Channel in Neurological Disorders.The Journal of membrane biology · 2021Review
- Carotid body chemoreceptors: physiology, pathology, and implications for health and disease.Physiological reviews · 2021Review
- Implication of Potassium Channels in the Pathophysiology of Pulmonary Arterial Hypertension.Biomolecules · 2020Review
- Effects of the ventilatory stimulant, doxapram on human TASK-3 (KCNK9, K2P9.1) channels and TASK-1 (KCNK3, K2P3.1) channels.Acta physiologica (Oxford, England) · 2020Article
- Characterization and regulation of wild-type and mutant TASK-1 two pore domain potassium channels indicated in pulmonary arterial hypertension.The Journal of physiology · 2019Article
- Much more than a leak: structure and function of K₂p-channels.Pflugers Archiv : European journal of physiology · 2015Review
- TASK channels in arterial chemoreceptors and their role in oxygen and acid sensing.Pflugers Archiv : European journal of physiology · 2015Review
- Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression: a new therapeutic concept.British journal of pharmacology · 2015Review
- Differential phospholipase C-dependent modulation of TASK and TREK two-pore domain K+ channels in rat thalamocortical relay neurons.The Journal of physiology · 2015Article
- Enhancement of TWIK-related acid-sensitive potassium channel 3 (TASK3) two-pore domain potassium channel activity by tumor necrosis factor α.The Journal of biological chemistry · 2014Article
- Intrinsic properties and neuropharmacology of midline paraventricular thalamic nucleus neurons.Frontiers in behavioral neuroscience · 2014Review
- A role for two-pore potassium (K2P) channels in endometrial epithelial function.Journal of cellular and molecular medicine · 2013Article
- International Union of Basic and Clinical Pharmacology. LXXIX. Cannabinoid receptors and their ligands: beyond CB₁ and CB₂.Pharmacological reviews · 2010Review
- Trafficking of neuronal two pore domain potassium channels.Current neuropharmacology · 2010Article
- Gating of two pore domain potassium channels.The Journal of physiology · 2010Review
- TRESK background K(+) channel is inhibited by phosphorylation via two distinct pathways.The Journal of biological chemistry · 2010Article
- Receptors and channels targeted by synthetic cannabinoid receptor agonists and antagonists.Current medicinal chemistry · 2010Review
- The response of the tandem pore potassium channel TASK-3 (K(2P)9.1) to voltage: gating at the cytoplasmic mouth.The Journal of physiology · 2009Article
- TASK1 modulates inflammation and neurodegeneration in autoimmune inflammation of the central nervous system.Brain : a journal of neurology · 2009Article
- Heteromeric TASK-1/TASK-3 is the major oxygen-sensitive background K+ channel in rat carotid body glomus cells.The Journal of physiology · 2009Article
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 3 institutions in 2 countries.
Funding
Abstract
background and purposeThe TASK subfamily of two pore domain potassium channels (K2P) encodes for leak K currents, contributing to the resting membrane potential of many neurons and regulating their excitability. TASK1 and TASK3 channels are regulated by a number of pharmacological and physiological mediators including cannabinoids such as methanandamide. In this study, we investigate how methanandamide blocks these channels. EXPERIMENTAL APPROACH: Currents through wild type and mutated TASK1 and TASK3 channels expressed in modified HEK-293 cells were measured using whole-cell electrophysiological recordings in the presence and absence of methanandamide. KEY
resultsMethanandamide (3 microM) produced substantial block of hTASK1, hTASK3 and mTASK3 channels but was most potent at blocking hTASK3 channels. Block of these channels was irreversible unless cells were washed with buffer containing bovine serum albumin. Mutation of the distal six amino acids of TASK1 did not alter methanandamide inhibition, whilst C terminal truncation of TASK3 channels caused a small but significant reduction of inhibition. However, deletion of six amino acids (VLRFLT) at the interface between the final transmembrane domain and cytoplasmic C terminus of TASK3 channels gave functional currents that were no longer inhibited by methanandamide or by activation of GPCRs. CONCLUSIONS AND IMPLICATIONS: Methanandamide potently blocked TASK3 and TASK1 channels and both methanandamide and G protein-mediated inhibition converged on the same intracellular gating pathway. Physiologically, methanandamide block of TASK1 and TASK3 channels may underpin a number of CNS effects of cannabinoids that are not mediated through activation of CB1 or CB2 receptors.
Indexed as
Identifiers
What OpenQuestion holds
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.