Aliases for SCN3B Gene
External Ids for SCN3B Gene
Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel beta subunit gene family, and influences the inactivation kinetics of the sodium channel. Two alternatively spliced variants, encoding the same protein, have been identified. [provided by RefSeq, Jul 2008]
GeneCards Summary for SCN3B Gene
SCN3B (Sodium Channel, Voltage Gated, Type III Beta Subunit) is a Protein Coding gene. Diseases associated with SCN3B include brugada syndrome 7 and brugada syndrome. Among its related pathways are L1CAM interactions and Activation of cAMP-Dependent PKA. GO annotations related to this gene include ion channel binding and voltage-gated sodium channel activity. An important paralog of this gene is SCN1B.
UniProtKB/Swiss-Prot for SCN3B Gene
Modulates channel gating kinetics. Causes unique persistent sodium currents. Inactivates the sodium channel opening more slowly than the subunit beta-1. Its association with neurofascin may target the sodium channels to the nodes of Ranvier of developing axons and retain these channels at the nodes in mature myelinated axons (By similarity).
Voltage-gated sodium channels (NaV) are responsible for action potential initiation and propagation in excitable cells, including nerve, muscle, and neuroendocrine cell types. They are also expressed at low levels in non-excitable cells, where their physiological role is unclear. Structurally, Nav channels are composed of one pore-forming alpha-subunit, which may be associated with either one or more beta-subunits. alpha-subunits are composed for four homologous domains, each of which contains six transmembrane segments. The fourth transmembrane loop (S4) acts as the voltage sensor and is activated by changes in membrane potential. S4 is also involved in channel gating.