Na Channel β1 Subunit (D9T5B) Rabbit mAb recognizes endogenous levels of total sodium channel β1 subunit protein. This antibody also cross-reacts with an unidentified protein of 60 kDa in whole brain lysate.

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala51 of human sodium channel β1 subunit protein.

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 β1 subunit (SCN1B) plays a crucial role in neuronal migration and pathfinding during brain development (14). Mutations in the corresponding SCN1B gene are associated with generalized epilepsy with febrile seizures plus 1 (15), Brugada syndrome (16), and familial atrial fibrillation (17). A SCN1B loss of function mutation results in a severe form of pediatric epileptic encephalopathy known as Dravet syndrome (18).