Potassium sodium-activated channel subfamily T member 1
genes
References
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 novogain-of-function KCNT1 channel mutations cause malignant migrating partialseizures of infancy. Nat Genet. 2012 Nov;44(11):1255-9. doi: 10.1038/ng.2441.
Bhattacharjee A, Kaczmarek LK. For K+ channels, Na+ is the new Ca2+. TrendsNeurosci. 2005 Aug;28(8):422-8. Review.
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 KCNT1cause severe autosomal dominant nocturnal frontal lobe epilepsy. Nat Genet. 2012 Nov;44(11):1188-90. doi: 10.1038/ng.2440.
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 caseswith malignant migrating partial seizures in infancy. Gene. 2013 Dec1;531(2):467-71. doi: 10.1016/j.gene.2013.08.096.
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.
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