The beta-2 subunit of the mammalian brain voltage-gated sodium channel, known as sodium channel subunit beta-2 (SCN2B) is a 186-residue glycoprotein that contains an extracellular N-terminal domain with similarity to the neural adhesion molecule contactin and a single transmembrane domain. The large alpha subunits of mammalian voltage-gated sodium channels can generate a functional channel when expressed alone in Xenopus oocytes, but the association with the beta-1 or beta-2 subunit has been shown to modify channel function. SCN2B is shown to be expressed in central neurons only, where covalent association with the alpha subunit is correlated with insertion into the cell membrane.
|Basic Information of SCN2B|
|Protein Name||Sodium channel subunit beta-2|
|Organism||Homo sapiens (Human)|
SCN2B can regulate channel gating, modulate channel expression and localization, and interact with the extracellular matrix molecules. Previous studies have demonstrated that this subunit is distributed in the central and peripheral nervous systems. SCN2B is expressed in hippocampal and cortical neurons, and cerebellar Purkinje neurons. In the dorsal root ganglion (DRG), SCN2B-containing neurons have various cell body sizes. SCN2B is thought to be associated with nociceptive transmission in the sensory ganglion of spinal nerves. However, little is known about the function of SCN2B in other sensory systems. Diseases associated with SCN2B include Brugada syndrome, atrial fibrillation, or sudden infant death syndrome. Among its related pathways are cardiac conduction and L1CAM interactions.
Fig.1 (A) Schematic representation of the α-subunits of cardiac sodium channel, consisting of 4 serially linked homologous domains (DI-DIV), each containing 6 transmembrane segments (S1-S6). (B) The interacting β-subunits and other regulatory proteins are depicted. (Wilde, 2011)
This article finds that SCN2B is expressed by TG neurons with various cell body sizes. SCN2B-IR nerve endings are also detected in association with vibrissae, guard hairs, mucosal epithelia and salivary ducts. The distribution and morphology of these endings suggest that they are sensory in nature and derived from the TG.
This article reveals several associations of SCN genes with epilepsy. Confirmation of the data in independent sets of samples will shed further light on these findings and would allow us to start collecting a list of common genetic variants that could be genotyped to determine the vulnerability of each individual to develop epilepsy.
This article suggests that only SCN2B displays expressional changes in the prefrontal cortex of SAMP8-8 and SAMP8-12m associated with age-related changes in the human prefrontal cortex.
This article reveals that a missense mutation in the SCN2B gene may be responsible for BrS by decreasing Nav1.5 cell surface expression with the concomitant reduction of INa.
This article suggests that several sodium channel genes involve the etiology of idiopathic epilepsy, including SCN1A, SCN2A.
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