SCN3A:SCN2B,4B transports Na+ from the extracellular region to the cytosol

Stable Identifier
R-HSA-9717374
Type
Reaction [transition]
Species
Homo sapiens
Compartment
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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).

Literature References
PubMed ID Title Journal Year
24157691 Novel SCN3A variants associated with focal epilepsy in children

Vanoye, CG, Gurnett, CA, Holland, KD, George, AL, Kearney, JA

Neurobiol Dis 2014
29466837 Mutations in SCN3A cause early infantile epileptic encephalopathy

Zaman, T, Helbig, I, Božović, IB, DeBrosse, SD, Bergqvist, AC, Wallis, K, Medne, L, Maver, A, Peterlin, B, Helbig, KL, Zhang, X, Goldberg, EM

Ann Neurol 2018
Participants
Output
Participates
Catalyst Activity

sodium channel activity of SCN3A:SCN2B,4B [plasma membrane]

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