SCN4B is a regulatory subunit of multiple voltage-gated sodium channels, which are also called VGSCs or VDSCs. Nav channels switch between closed and open conformations depending on the voltage difference across the membrane. In the open state they let Na+ ions pass selectively through the pore, down their electrochemical gradient. The resulting influx depolarises the membrane and starts the propagation of electrical signals through cells and tissues. As an accessory beta subunit, SCN4B takes part in the localisation and functional modulation of these channels. It modulates the activity of SCN1A (Nav1.1) and SCN2A (Nav1.2).

The SCN4B gene encodes one of several sodium channel beta subunits. These subunits interact with voltage-gated alpha subunits to change sodium channel kinetics. The encoded protein is a transmembrane protein that sits in the cell membrane, and it forms interchain disulfide bonds with SCN2A. HGNC classes it among the V-set domain containing proteins and the sodium voltage-gated channel beta subunits, and UniProt places it in the sodium channel auxiliary subunit SCN4B family. Three protein-coding transcript variants and one non-coding variant have been reported for the gene. Mouse and rat both have an Scn4b ortholog.

Defects in the SCN4B gene are a cause of long QT syndrome type 10, which explains the alias LQT10. Earlier names for the gene include sodium channel, voltage-gated, type IV, beta subunit. Researchers studying the SCN4B protein often do so alongside other sodium channel subunits, to understand how auxiliary subunits shape channel behaviour in excitable tissues.