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Scn2b is a member of voltage-gated sodium channels (NaV) that are responsible for action potential initiation and propagation in excitable cells, including nerve, muscle, and neuroendocrine cell types. Scn2b are also expressed at low levels in non-excitable cells, where their physiological role is unclear. Scn2b is crucial in the assembly, expression, and functional modulation of the heterotrimeric complex of the sodium channel. In Scn2b, the subunit beta-2 causes an increase in the plasma membrane surface area and in its folding into microvilli. Also, Scn2b interacts with TNR (Tenascin R-precursor) and may play a crucial role in clustering and regulation of activity of sodium channels at nodes of Ranvier. The protein encoded by the Scn2b gene is the beta 2 subunit of the type II voltage-gated sodium channel. Scn2b protein is involved in cell-cell adhesion and cell migration. Defects in the Scn2b gene can be a cause of Brugada Syndrome, atrial fibrillation, or sudden infant death syndrome. Diseases associated with SCN2B include Atrial Fibrillation, Familial, 14 and Scn2b-Related Familial Atrial Fibrillation.
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