SCN3A in combination with a regulatory beta subunit responds to depolarization by opening and passively transporting sodium ions according to the concentration gradient from the extracellular region to the cytosol (Vanoye et al. 2014, Zaman et al. 2018). In mouse type II taste cells, initial depolarization at the apex of the cell is believed to cause an activation potential via Scn2a, Scn3a, and Scn9a located at the basolateral membrane (Gao et al. 2009). Mutations in SCN3A cause infantile epilepsy (Vanoye et al. 2014, Zaman et al. 2018).
Maver, A, Goldberg, EM, Božović, IB, Helbig, I, Zaman, T, Peterlin, B, Wallis, K, Medne, L, Bergqvist, AC, Zhang, X, Helbig, KL, DeBrosse, SD
Vanoye, CG, George, AL, Holland, KD, Gurnett, CA, Kearney, JA
sodium channel activity of SCN3A:SCN2B,4B [plasma membrane]
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