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The sodium channel protein beta-4 subunit (SCN4B) is a non-pore-forming auxiliary subunit of voltage-gated sodium channels, encoded by the SCN4B gene[1][5]. It belongs to a family of auxiliary β subunits (β1–β4), which modulate the biophysical properties, trafficking, and localization of sodium channel α subunits[1][2][5]. The β4 subunit contains an extracellular immunoglobulin-like (Ig) domain, making it part of the Ig superfamily of cell adhesion molecules[1][3][5]. In addition to its classical modulatory role, SCN4B participates in cell adhesion, neuronal development, and may interact with extracellular matrix and cytoskeletal components[1][3][5]. Mutations in SCN4B have been linked to pathologies including epilepsy, cardiac arrhythmias, neuropathic pain, cancer, and neurodegenerative disorders, highlighting its therapeutic relevance[1][5]. The β4 subunit can alter the sensitivity and pharmacological profile of sodium channels, and its structural properties (e.g., formation of disulfide bonds) are essential for its modulatory function[3][5].
Modulation of sodium channel function, Alteration of channel kinetics, Indirect modulation by channel-blocking toxins
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