Target intelligence / Profile preview

Sodium channel protein beta-4 subunit (SCN4B)

Target
SCN4B
Molecular classification
Ion channel auxiliary subunit, Immunoglobulin superfamily, Cell adhesion molecule
01

Overview

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].

Other names
sodium voltage-gated channel beta subunit 4sodium channel β4 subunitNavβ4SCN4B
02

Mechanism of action

Modulation of sodium channel function, Alteration of channel kinetics, Indirect modulation by channel-blocking toxins

03

Biological functions

Modulation of sodium channel gating kineticsCell adhesionRegulation of neuronal excitabilityNeurite outgrowthNeuronal pathfinding
04

Disease associations

EpilepsyCardiac arrhythmiaNeurodegenerative diseaseSudden unexpected death in epilepsyCancerNeuropathic pain
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Safety considerations

Mutations in SCN4B and related β subunit genes can be associated with risk of cardiac arrhythmia, epilepsy, and other channelopathies[1][3][5].

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