Na Channel β2 Subunit (D6L5Y) Rabbit mAb #13966

Mammalian voltage-gated sodium channels (VGSCs) are composed of a pore-forming α subunit and one or more regulatory β subunits (1). Four separate genes (SCN1B-SCN4B) encode the five mammalian β subunits β1, β1B, β2, β3, and β4. In general, β subunit proteins are type I transmembrane proteins, with the exception of secreted β1B protein (reviewed in 2). β subunits regulate α subunit gating and kinetics, which controls cell excitability (3,4). Sodium channel β subunits also function as Ig superfamily cell adhesion molecules that regulate cell adhesion and migration (5,6). Additional research reveals sequential processing of β subunit proteins by β-secretase (BACE1) and γ secretase, resulting in ectodomain shedding of β subunit and generation of an intracellular carboxy-terminal fragment (CTF). Generation of the CTF is thought to play a role in cell adhesion and migration (7,8). Multiple studies demonstrate a link between β subunit gene mutations and a number of disorders, including epilepsy, cardiac arrhythmia, multiple sclerosis, neuropsychiatric disorders, neuropathy, inflammatory pain, and cancer (9-13).
The sodium channel β2 subunit (SCN2B) plays a role in the assembly and functioning of cell surface sodium channels (14). Mutations in the corresponding SCN2B gene may be associated with a form of atrial fibrillation and at least one identified case of Brugada syndrome (15,16). Research using a rat model of spared nerve injury (SNI) suggests that the β2 subunit may be involved in the generation of neuropathic pain (17).