Potassium channel subfamily K member 9 is aprotein that in humans is encoded by theKCNK9gene.[4][5][6]
This gene encodes K2P9.1, one of the members of the superfamily of potassium channel proteins containing two pore-forming P domains. This open channel is highly expressed in the cerebellum. It is inhibited by extracellular acidification andarachidonic acid, and strongly inhibited by phorbol 12-myristate 13-acetate.[6][7] Phorbol 12-myristate 13-acetate is also known as12-O-tetradecanoylphorbol-13-acetate (TPA). TASK channels are additionally inhibited by hormones and transmitters that signal through GqPCRs. The resulting cellular depolarization is thought to regulate processes such as motor control andaldosterone secretion. Despite early controversy about the exact mechanism underlying this inhibition, the current view is thatDiacyl-glycerol, produced by the breakdown ofPhosphatidylinositol-4,5-bis-phosphate byPhospholipase Cβ causes channel closure.[8]
The KCNK9 gene is expressed as an ion channel more commonly known as TASK 3. This channel has a varied pattern of expression. TASK 3 is coexpressed with TASK 1 (KCNK3) in the cerebellar granule cells, locus coeruleus, motor neurons, pontine nuclei, some cells in the neocortex, habenula, olfactory bulb granule cells, and cells in the external plexiform layer of the olfactory bulb.[9] TASK-3 channels are also expressed in the hippocampus; both on pyramidal cells and interneurons.[10] It is thought that these channels may form heterodimers where their expressions co-localise.[11][12]
Mice in which the TASK-3 gene has been deleted have reduced sensitivity to inhalation anaesthetics, exaggerated nocturnal activity and cognitive deficits as well as significantly increased appetite and weight gain.[13][14] A role for TASK-3 channels in neuronal network oscillations has also been described: TASK-3 knockout mice lack the atropine-sensitive halothane-induced theta oscillation (4–7 Hz) from the hippocampus and are unable to maintain theta oscillations during rapid eye movement (REM) sleep.[14]
^Bayliss DA, Sirois JE, Talley EM (June 2003). "The TASK family: two-pore domain background K+ channels".Molecular Interventions.3 (4):205–219.doi:10.1124/mi.3.4.205.PMID14993448.
^Linden AM, Aller MI, Leppä E, Rosenberg PH, Wisden W, Korpi ER (October 2008). "K+ channel TASK-1 knockout mice show enhanced sensitivities to ataxic and hypnotic effects of GABA(A) receptor ligands".The Journal of Pharmacology and Experimental Therapeutics.327 (1):277–286.doi:10.1124/jpet.108.142083.PMID18660435.S2CID31086459.
Chapman CG, Meadows HJ, Godden RJ, Campbell DA, Duckworth M, Kelsell RE, et al. (2001). "Cloning, localisation and functional expression of a novel human, cerebellum specific, two pore domain potassium channel".Brain Research. Molecular Brain Research.82 (1–2):74–83.doi:10.1016/S0169-328X(00)00183-2.PMID11042359.
Vega-Saenz de Miera E, Lau DH, Zhadina M, Pountney D, Coetzee WA, Rudy B (2001). "KT3.2 and KT3.3, two novel human two-pore K(+) channels closely related to TASK-1".Journal of Neurophysiology.86 (1):130–142.doi:10.1152/jn.2001.86.1.130.PMID11431495.S2CID14855672.
Kim CJ, Cho YG, Jeong SW, Kim YS, Kim SY, Nam SW, et al. (2005). "Altered expression of KCNK9 in colorectal cancers".APMIS: Acta Pathologica, Microbiologica, et Immunologica Scandinavica.112 (9):588–594.doi:10.1111/j.1600-0463.2004.apm1120905.x.PMID15601307.S2CID41751315.
