KCNK4

KCNK4
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
Aliases KCNK4, K2p4.1, TRAAK, TRAAK1, potassium two pore domain channel subfamily K member 4
External IDs MGI: 1298234 HomoloGene: 7391 GeneCards: KCNK4
Targeted by Drug
riluzole[1]
RNA expression pattern
More reference expression data
Orthologs
Species Human Mouse
Entrez

50801

16528

Ensembl

ENSG00000182450

ENSMUSG00000024957

UniProt

Q9NYG8

O88454

RefSeq (mRNA)

NM_016611
NM_033310
NM_001317090

NM_008431

RefSeq (protein)

NP_201567.1
NP_001304019.1

NP_032457.1

Location (UCSC) Chr 11: 64.29 – 64.3 Mb Chr 19: 6.93 – 6.93 Mb
PubMed search [2] [3]
Wikidata
View/Edit HumanView/Edit Mouse

Potassium channel subfamily K member 4 is a protein that in humans is encoded by the KCNK4 gene.[4][5][6]

Function

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 the K2P4.1 protein, one of the members of the superfamily of potassium channel proteins containing two pore-forming P domains. K2P4.1 homodimerizes and functions as an outwardly rectifying channel. It is expressed primarily in neural tissues and is stimulated by membrane stretch and polyunsaturated fatty acids.[6]

KCNK4 protein channels are also called TRAAK channels. TRAAK channels are found in mammalian neurons and are part of a protein family of weakly inward rectifying potassium channels. This subfamily of potassium channels is mechanically gated. The C-terminal of TRAAK has a charged cluster that is important in maintaining the mechanosensitive properties of the channel.[7]

TRAAK is only expressed in neuronal tissue, and can be found in the brain, spinal cord, and retina, which suggests that it has a function beyond mechanotransduction in terms of neuronal excitability.[8] The highest levels of TRAAK expression are in the olfactory system, cerebral cortex, hippocampal formation, habenula, basal ganglia, and cerebellum.[8] TRAAK channels are mechanically activated when there is a convex curvature in the membrane that alters the channel’s activity. TRAAK channels are thought to have a role in axonal pathfinding, growth cone motility, and neurite elongation, as well as possibly having a role in touch or pain detection.[9][10]

See also

References

  1. "Drugs that physically interact with Potassium channel subfamily K member 4 view/edit references on wikidata".
  2. "Human PubMed Reference:".
  3. "Mouse PubMed Reference:".
  4. Lesage F, Maingret F, Lazdunski M (May 2000). "Cloning and expression of human TRAAK, a polyunsaturated fatty acids-activated and mechano-sensitive K(+) channel". FEBS Lett. 471 (2–3): 137–40. doi:10.1016/S0014-5793(00)01388-0. PMID 10767409.
  5. Goldstein SA, Bayliss DA, Kim D, Lesage F, Plant LD, Rajan S (Dec 2005). "International Union of Pharmacology. LV. Nomenclature and molecular relationships of two-P potassium channels". Pharmacol Rev. 57 (4): 527–40. doi:10.1124/pr.57.4.12. PMID 16382106.
  6. 1 2 "Entrez Gene: KCNK4 potassium channel, subfamily K, member 4".
  7. Patel AJ, Honoré E, Lesage F, Fink M, Romey G, Lazdunski M (1999). "Inhalational anesthetics activate two-pore-domain background K+ channels". Nature Neuroscience. 2 (5): 422–426. doi:10.1038/8084. PMID 10321245.
  8. 1 2 Fink M, Lesage F, Duprat F, Heurteaux C, Reyes R, Fosset M, Lazdunski M (1998). "A neuronal two P domain K+ channel stimulated by arachidonic acid and polyunsaturated fatty acids". The EMBO Journal. 17 (12): 3297–3308. doi:10.1093/emboj/17.12.3297. PMC 1170668Freely accessible. PMID 9628867.
  9. Vandorpe DH, Morris CE (1992). "Stretch activation of the Aplysia S-channel". The Journal of membrane biology. 127 (3): 205–214. PMID 1495087.
  10. Maingret F, Fosset M, Lesage F, Lazdunski M, Honoré E (1999). "TRAAK is a mammalian neuronal mechano-gated K+ channel". The Journal of Biological Chemistry. 274 (3): 1381–1387. doi:10.1074/jbc.274.3.1381. PMID 9880510.

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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