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Summary Expression Phenotypes Gene Literature (34) GO Terms (5) Nucleotides (48) Proteins (30) Interactants (59) Wiki
XB-GENEPAGE-6257491

Papers associated with kcnk18



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Critical contribution of the intracellular C-terminal region to TRESK channel activity is revealed by the epithelial Na+ current ratio method., Debreczeni D, Baukál D, Pergel E, Veres I, Czirják G., J Biol Chem. June 1, 2023; 299 (6): 104737.                        


Validation of TREK1 ion channel activators as an immunomodulatory and neuroprotective strategy in neuroinflammation., Schroeter CB, Nelke C, Schewe M, Spohler L, Herrmann AM, Müntefering T, Huntemann N, Kuzikov M, Gribbon P, Albrecht S, Bock S, Hundehege P, Neelsen LC, Baukrowitz T, Seebohm G, Wünsch B, Bittner S, Ruck T, Budde T, Meuth SG., Biol Chem. March 28, 2023; 404 (4): 355-375.              


KCNK18 Biallelic Variants Associated with Intellectual Disability and Neurodevelopmental Disorders Alter TRESK Channel Activity., Pavinato L, Nematian-Ardestani E, Zonta A, De Rubeis S, Buxbaum J, Mancini C, Bruselles A, Tartaglia M, Pessia M, Tucker SJ, D'Adamo MC, Brusco A., Int J Mol Sci. June 4, 2021; 22 (11):         


TRESK and TREK-2 two-pore-domain potassium channel subunits form functional heterodimers in primary somatosensory neurons., Lengyel M, Czirják G, Jacobson DA, Enyedi P., J Biol Chem. August 28, 2020; 295 (35): 12408-12425.                      


Altered functional properties of a missense variant in the TRESK K+ channel (KCNK18) associated with migraine and intellectual disability., Imbrici P, Nematian-Ardestani E, Hasan S, Pessia M, Tucker SJ, D'Adamo MC., Pflugers Arch. July 1, 2020; 472 (7): 923-930.


Chemically Modified Derivatives of the Activator Compound Cloxyquin Exert Inhibitory Effect on TRESK (K2P18.1) Background Potassium Channel., Lengyel M, Erdélyi F, Pergel E, Bálint-Polonka Á, Dobolyi A, Bozsaki P, Dux M, Király K, Hegedűs T, Czirják G, Mátyus P, Enyedi P., Mol Pharmacol. June 1, 2019; 95 (6): 652-660.


TRESK (K2P18.1) Background Potassium Channel Is Activated by Novel-Type Protein Kinase C via Dephosphorylation., Pergel E, Lengyel M, Enyedi P, Czirják G., Mol Pharmacol. June 1, 2019; 95 (6): 661-672.


Migraine-Associated TRESK Mutations Increase Neuronal Excitability through Alternative Translation Initiation and Inhibition of TREK., Royal P, Andres-Bilbe A, Ávalos Prado P, Verkest C, Wdziekonski B, Schaub S, Baron A, Lesage F, Gasull X, Levitz J, Sandoz G., Neuron. January 16, 2019; 101 (2): 232-245.e6.


Anesthetic-sensitive ion channel modulation is associated with a molar water solubility cut-off., Brosnan RJ, Pham TL., BMC Pharmacol Toxicol. September 14, 2018; 19 (1): 57.                


TRESK background potassium channel is not gated at the helix bundle crossing near the cytoplasmic end of the pore., Lengyel M, Czirják G, Enyedi P., PLoS One. May 15, 2018; 13 (5): e0197622.          


Selective and state-dependent activation of TRESK (K2P 18.1) background potassium channel by cloxyquin., Lengyel M, Dobolyi A, Czirják G, Enyedi P., Br J Pharmacol. July 1, 2017; 174 (13): 2102-2113.


The Effect of Pungent and Tingling Compounds from Piper nigrum L. on Background K+ Currents., Beltrán LR, Dawid C, Beltrán M, Levermann J, Titt S, Thomas S, Pürschel V, Satalik M, Gisselmann G, Hofmann T, Hatt H., Front Pharmacol. May 26, 2017; 8 408.                


PTH1R Mutants Found in Patients with Primary Failure of Tooth Eruption Disrupt G-Protein Signaling., Subramanian H, Döring F, Kollert S, Rukoyatkina N, Sturm J, Gambaryan S, Stellzig-Eisenhauer A, Meyer-Marcotty P, Eigenthaler M, Wischmeyer E., PLoS One. November 1, 2016; 11 (11): e0167033.          


Properties, regulation, pharmacology, and functions of the K₂p channel, TRESK., Enyedi P, Czirják G., Pflugers Arch. May 1, 2015; 467 (5): 945-58.


Differential sensitivity of TREK-1, TREK-2 and TRAAK background potassium channels to the polycationic dye ruthenium red., Braun G, Lengyel M, Enyedi P, Czirják G., Br J Pharmacol. April 1, 2015; 172 (7): 1728-38.


Hydroxy-α sanshool induces colonic motor activity in rat proximal colon: a possible involvement of KCNK9., Kubota K, Ohtake N, Ohbuchi K, Mase A, Imamura S, Sudo Y, Miyano K, Yamamoto M, Kono T, Uezono Y., Am J Physiol Gastrointest Liver Physiol. April 1, 2015; 308 (7): G579-90.                  


Activation of TRESK channels by the inflammatory mediator lysophosphatidic acid balances nociceptive signalling., Kollert S, Dombert B, Döring F, Wischmeyer E., Sci Rep. January 12, 2015; 5 12548.            


Nonmigraine-associated TRESK K+ channel variant C110R does not increase the excitability of trigeminal ganglion neurons., Guo Z, Liu P, Ren F, Cao YQ., J Neurophysiol. August 1, 2014; 112 (3): 568-79.


Direct action and modulating effect of (+)- and (-)-nicotine on ion channels expressed in trigeminal sensory neurons., Schreiner BS, Lehmann R, Thiel U, Ziemba PM, Beltrán LR, Sherkheli MA, Jeanbourquin P, Hugi A, Werner M, Gisselmann G, Hatt H., Eur J Pharmacol. April 5, 2014; 728 48-58.


Functional characterization of zebrafish K2P18.1 (TRESK) two-pore-domain K+ channels., Rahm AK, Wiedmann F, Gierten J, Schmidt C, Schweizer PA, Becker R, Katus HA, Thomas D., Naunyn Schmiedebergs Arch Pharmacol. March 1, 2014; 387 (3): 291-300.


Functional analysis of a migraine-associated TRESK K+ channel mutation., Liu P, Xiao Z, Ren F, Guo Z, Chen Z, Zhao H, Cao YQ., J Neurosci. July 31, 2013; 33 (31): 12810-24.


The pungent substances piperine, capsaicin, 6-gingerol and polygodial inhibit the human two-pore domain potassium channels TASK-1, TASK-3 and TRESK., Beltrán LR, Dawid C, Beltrán M, Gisselmann G, Degenhardt K, Mathie K, Hofmann T, Hatt H., Front Pharmacol. January 1, 2013; 4 141.              


TRESK background K(+) channel is inhibited by PAR-1/MARK microtubule affinity-regulating kinases in Xenopus oocytes., Braun G, Nemcsics B, Enyedi P, Czirják G., PLoS One. January 1, 2011; 6 (12): e28119.            


TRESK background K(+) channel is inhibited by phosphorylation via two distinct pathways., Czirjak G, Enyedi P., J Biol Chem. May 7, 2010; 285 (19): 14549-57.


N-linked glycosylation determines cell surface expression of two-pore-domain K+ channel TRESK., Egenberger B, Polleichtner G, Wischmeyer E, Döring F., Biochem Biophys Res Commun. January 8, 2010; 391 (2): 1262-7.


Phosphorylation-dependent binding of 14-3-3 proteins controls TRESK regulation., Czirják G, Vuity D, Enyedi P., J Biol Chem. June 6, 2008; 283 (23): 15672-80.


TRESK two-pore-domain K+ channels constitute a significant component of background potassium currents in murine dorsal root ganglion neurones., Dobler T, Springauf A, Tovornik S, Weber M, Schmitt A, Sedlmeier R, Wischmeyer E, Döring F., J Physiol. December 15, 2007; 585 (Pt 3): 867-79.


Anesthetic properties of the ketone bodies beta-hydroxybutyric acid and acetone., Yang L, Zhao J, Milutinovic PS, Brosnan RJ, Eger EI, Sonner JM., Anesth Analg. September 1, 2007; 105 (3): 673-9.


Ammonia has anesthetic properties., Brosnan RJ, Yang L, Milutinovic PS, Zhao J, Laster MJ, Eger EI, Sonner JM., Anesth Analg. June 1, 2007; 104 (6): 1430-3, table of contents.


Chirality in anesthesia II: stereoselective modulation of ion channel function by secondary alcohol enantiomers., Brosnan R, Gong D, Cotten J, Keshavaprasad B, Yost CS, Eger EI, Sonner JM., Anesth Analg. July 1, 2006; 103 (1): 86-91, table of contents.


Targeting of calcineurin to an NFAT-like docking site is required for the calcium-dependent activation of the background K+ channel, TRESK., Czirják G, Enyedi P., J Biol Chem. May 26, 2006; 281 (21): 14677-82.


Zinc and mercuric ions distinguish TRESK from the other two-pore-domain K+ channels., Czirják G, Enyedi P., Mol Pharmacol. March 1, 2006; 69 (3): 1024-32.


Potent activation of the human tandem pore domain K channel TRESK with clinical concentrations of volatile anesthetics., Liu C, Au JD, Zou HL, Cotten JF, Yost CS., Anesth Analg. December 1, 2004; 99 (6): 1715-1722.


The two-pore domain K+ channel, TRESK, is activated by the cytoplasmic calcium signal through calcineurin., Czirják G, Tóth ZE, Enyedi P., J Biol Chem. April 30, 2004; 279 (18): 18550-8.

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