Potassium two pore domain channel subfamily K member 9
genes
References
Bando Y, Hirano T, Tagawa Y. Dysfunction of KCNK potassium channels impairsneuronal migration in the developing mouse cerebral cortex. Cereb Cortex. 2014Apr;24(4):1017-29. doi: 10.1093/cercor/bhs387.
Barel O, Shalev SA, Ofir R, Cohen A, Zlotogora J, Shorer Z, Mazor G, Finer G, Khateeb S, Zilberberg N, Birk OS. Maternally inherited Birk Barel mentalretardation dysmorphism syndrome caused by a mutation in the genomicallyimprinted potassium channel KCNK9. Am J Hum Genet. 2008 Aug;83(2):193-9. doi:10.1016/j.ajhg.2008.07.010.
Enyedi P, Czirják G. Molecular background of leak K+ currents: two-pore domainpotassium channels. Physiol Rev. 2010 Apr;90(2):559-605. doi:10.1152/physrev.00029.2009. Review.
Graham JM Jr, Zadeh N, Kelley M, Tan ES, Liew W, Tan V, Deardorff MA, WilsonGN, Sagi-Dain L, Shalev SA. KCNK9 imprinting syndrome-further delineation of apossible treatable disorder. Am J Med Genet A. 2016 Oct;170(10):2632-7. doi:10.1002/ajmg.a.37740.
Molecular Biology of the Cell (fourth edition, 2002): The Membrane Potential in Animal Cells Depends Mainly on K+ Leak Channels and the K+ Gradient Across the Plasma Membrane
Veale EL, Hassan M, Walsh Y, Al-Moubarak E, Mathie A. Recovery of currentthrough mutated TASK3 potassium channels underlying Birk Barel syndrome. MolPharmacol. 2014 Mar;85(3):397-407. doi: 10.1124/mol.113.090530.
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