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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Potassium channel, subfamily K, member 18

TRESK, TWIK-related spinal cord K+ channel, TRESK-2, KCNK18
Potassium channels play a role in many cellular processes including maintenance of the action potential, muscle contraction, hormone secretion, osmotic regulation, and ion flow. This gene encodes a member of the superfamily of potassium channel proteins containing two pore-forming P domains and the encoded protein functions as an outward rectifying potassium channel. A mutation in this gene has been found to be associated with migraine with aura.[provided by RefSeq, Jan 2011] (from NCBI)
Top mentioned proteins: K2P, TREK-1, ACID, TASK-3, Aura
Papers on TRESK
Genetic studies of Polish migraine patients: screening for causative mutations in four migraine-associated genes.
Kamińska et al., Warsaw, Poland. In Hum Genomics, Dec 2015
Recently, several mutations in KCNK18 have also been found as causative factors in migraine development.
Role of leak potassium channels in pain signaling.
Toyoda et al., China. In Brain Res Bull, Oct 2015
In this review, we describe evidence for the roles of TASK1, TASK3, TREK1, TREK2, TRAAK and TRESK channels in pain signaling and behavior.
TWIK-Related Spinal Cord K⁺ Channel Expression Is Increased in the Spinal Dorsal Horn after Spinal Nerve Ligation.
Lee et al., Taejŏn, South Korea. In Yonsei Med J, Sep 2015
PURPOSE: The TWIK-related spinal cord K⁺ channel (TRESK) has recently been discovered and plays an important role in nociceptor excitability in the pain pathway.
Emerging potassium channel targets for the treatment of pain.
Tsantoulas, London, United Kingdom. In Curr Opin Support Palliat Care, Jun 2015
Genetic analyses illustrate that K+ channel gene variation can predict pain sensitivity (KCNS1, GIRKs), risk for persistent pain (KCNS1, GIRKs, TRESK) and analgesic effectiveness (GIRK2).
Two-pore domain potassium channels: potential therapeutic targets for the treatment of pain.
Veale et al., Chatham, United Kingdom. In Pflugers Arch, May 2015
Expression of several different K2P channel subunits has been detected in nociceptive dorsal root ganglion neurons and trigeminal ganglion neurons, in particular, TREK1, TREK2, TRESK, TRAAK, TASK3 and TWIK1 channels.
Properties, regulation, pharmacology, and functions of the K₂p channel, TRESK.
Czirják et al., Budapest, Hungary. In Pflugers Arch, May 2015
TWIK-related spinal cord K(+) channel (TRESK) is the gene product of KCNK18, the last discovered leak potassium K2P channel gene.
Hydroxy-α sanshool induces colonic motor activity in rat proximal colon: a possible involvement of KCNK9.
Uezono et al., Ibaraki, Japan. In Am J Physiol Gastrointest Liver Physiol, May 2015
Hydroxy-α sanshool (HAS), a readily absorbable active ingredient of TU-100 and a KCNK3/KCNK9/KCNK18 blocker as well as TRPV1/TRPA1 agonist, has been investigated for its effects on colonic motility.
Differential sensitivity of TREK-1, TREK-2 and TRAAK background potassium channels to the polycationic dye ruthenium red.
Czirják et al., Budapest, Hungary. In Br J Pharmacol, Apr 2015
DRG neurons predominantly express TREK-2 and RR-resistant TREK-1 and TRESK (K2 P 18.1) background K(+) channels.
Activation of TRESK channels by the inflammatory mediator lysophosphatidic acid balances nociceptive signalling.
Wischmeyer et al., Würzburg, Germany. In Sci Rep, 2014
In dorsal root ganglia (DRG) neurons TRESK channels constitute a major current component of the standing outward current IKSO.
Differential expression of two-pore domain potassium channels in rat cerebellar granule neurons.
Zúñiga et al., Talca, Chile. In Biochem Biophys Res Commun, 2014
The presence of the major K2P subunits expressed was then confirmed by Western blot and immunofluorescence analysis, demonstrating robust expression of K2P1 (TWIK-1), K2P3 (TASK-1), K2P9 (TASK-3) and K2P18 (TRESK) channel protein.
The LQLP calcineurin docking site is a major determinant of the calcium-dependent activation of human TRESK background K+ channel.
Enyedi et al., Budapest, Hungary. In J Biol Chem, 2014
Calcium-dependent activation of human TRESK (TWIK-related spinal cord K(+) channel, K2P18.1)
KCNK18 (TRESK) genetic variants in Italian patients with migraine.
Dalla Volta et al., Torino, Italy. In Headache, 2014
BACKGROUND: A role for the KCNK18 gene encoding for TRESK, a member of the family of potassium channel, has been recently suggested in migraine with aura.
Migraine genetics: Part II.
Dodick et al., Philadelphia, United States. In Headache, 2013
TWIK-related spinal cord potassium channel is involved in migraine by screening the KCNK18 gene in subjects diagnosed with migraine.
TRESK: the lone ranger of two-pore domain potassium channels.
Czirják et al., Budapest, Hungary. In Mol Cell Endocrinol, 2012
dominant-negative mutation of human TRESK was found to be linked to migraine with aura in a large pedigree. It is hoped that future TRESK agonists may prevent or ameliorate the debilitating symptoms of migraine.
Migraine: Role of the TRESK two-pore potassium channel.
Rouleau et al., Montréal, Canada. In Int J Biochem Cell Biol, 2011
A frameshift mutation in the two-pore potassium channel protein TRESK is linked to migraine pathogenesis. (Review)
A dominant-negative mutation in the TRESK potassium channel is linked to familial migraine with aura.
Rouleau et al., Montréal, Canada. In Nat Med, 2010
a role for TRESK in the pathogenesis of typical migraine with aura.
Molecular background of leak K+ currents: two-pore domain potassium channels.
Czirják et al., Budapest, Hungary. In Physiol Rev, 2010
Basic physicochemical parameters (e.g., pH, temperature, membrane stretch) and also several intracellular signaling pathways substantially and specifically modulate the different members of the six K(2P) channel subfamilies (TWIK, TREK, TASK, TALK, THIK, and TRESK).
N-linked glycosylation determines cell surface expression of two-pore-domain K+ channel TRESK.
Döring et al., Würzburg, Germany. In Biochem Biophys Res Commun, 2010
single residue of TRESK was found to be glycosylated upon heterologous expression. Signals of the N-glycosylation mutants were reduced by >50% because of inadequate surface expression of the channel.
Regional expression of the anesthetic-activated potassium channel TRESK in the rat nervous system.
Yost et al., San Francisco, United States. In Neurosci Lett, 2009
These results provide an anatomic basis for identifying functional roles of TRESK in the rat nervous system.
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