potassium sodium-activated channel subfamily T member 1
Last updated 4 Aug 2025
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The KCNT1 gene belongs to a large family of genes that provide instructions for making potassium channels. These channels, which transport positively charged atoms (ions) of potassium into and out of cells, play a key role in a cell's ability to generate and transmit electrical signals.
Normal function
The KCNT1 gene belongs to a large family of genes that provide instructions for making potassium channels. These channels, which transport positively charged atoms (ions) of potassium into and out of cells, play a key role in a cell's ability to generate and transmit electrical signals.
Potassium channels are made up of several protein components (subunits). Each channel contains four alpha subunits that form the hole (pore) through which potassium ions move. Potassium channels can be made from four alpha subunits produced from the KCNT1 gene, or they can be made from subunits produced from both the KCNT1 gene and another gene called the KCNT2 gene.
The specific function of a potassium channel depends on its protein components and its location in the body. Channels that are made with the KCNT1 protein are active in nerve cells (neurons) in the brain, where they transport potassium ions out of cells. This flow of ions helps generate currents that activate (excite) neurons and send signals in the brain.
Researchers have determined that a molecule called PKC can increase the activity of channels that are made with the KCNT1 protein. While these channels can generate electrical currents without PKC, the currents are stronger when PKC attaches to the channel and increases the channel's activity.
Conditions referring to this gene or chromosome
Other names
KCa4.1
KIAA1422
potassium channel, sodium activated subfamily T, member 1
potassium channel, subfamily T, member 1
SLACK
Slo2.2
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Further reading and references
- potassium sodium-activated channel subfamily T member 1; MedlinePlus, National Library of Medicine.
- Barcia G, Fleming MR, Deligniere A, Gazula VR, Brown MR, Langouet M, Chen H, Kronengold J, Abhyankar A, Cilio R, Nitschke P, Kaminska A, Boddaert N, Casanova JL, Desguerre I, Munnich A, Dulac O, Kaczmarek LK, Colleaux L, Nabbout R. De novo gain-of-function KCNT1 channel mutations cause malignant migrating partial seizures of infancy. Nat Genet. 2012 Nov;44(11):1255-9. doi: 10.1038/ng.2441. Epub 2012 Oct 21.
- Bhattacharjee A, Kaczmarek LK. For K+ channels, Na+ is the new Ca2+. Trends Neurosci. 2005 Aug;28(8):422-8. doi: 10.1016/j.tins.2005.06.003.
- Gertler T, Bearden D, Bhattacharjee A, Carvill G. KCNT1-Related Epilepsy. 2018 Sep 20. In: Adam MP, Bick S, Mirzaa GM, Wallace SE, Amemiya A, editors. GeneReviews(R) [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from http://www.ncbi.nlm.nih.gov/books/NBK525917/
- Heron SE, Smith KR, Bahlo M, Nobili L, Kahana E, Licchetta L, Oliver KL, Mazarib A, Afawi Z, Korczyn A, Plazzi G, Petrou S, Berkovic SF, Scheffer IE, Dibbens LM. Missense mutations in the sodium-gated potassium channel gene KCNT1 cause severe autosomal dominant nocturnal frontal lobe epilepsy. Nat Genet. 2012 Nov;44(11):1188-90. doi: 10.1038/ng.2440. Epub 2012 Oct 21.
- Ishii A, Shioda M, Okumura A, Kidokoro H, Sakauchi M, Shimada S, Shimizu T, Osawa M, Hirose S, Yamamoto T. A recurrent KCNT1 mutation in two sporadic cases with malignant migrating partial seizures in infancy. Gene. 2013 Dec 1;531(2):467-71. doi: 10.1016/j.gene.2013.08.096. Epub 2013 Sep 10.
- Kurahashi H, Hirose S. Autosomal Dominant Sleep-Related Hypermotor (Hyperkinetic) Epilepsy. 2002 May 16 [updated 2023 Mar 23]. In: Adam MP, Bick S, Mirzaa GM, Wallace SE, Amemiya A, editors. GeneReviews(R) [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from http://www.ncbi.nlm.nih.gov/books/NBK1169/
- Santi CM, Ferreira G, Yang B, Gazula VR, Butler A, Wei A, Kaczmarek LK, Salkoff L. Opposite regulation of Slick and Slack K+ channels by neuromodulators. J Neurosci. 2006 May 10;26(19):5059-68. doi: 10.1523/JNEUROSCI.3372-05.2006.
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