Overview
- Peptide CKRRSETTAETFTE, corresponding to amino acid residues 43-56 of rat β1 subunit of voltage-gated Na+ channels (Accession Q00954). Extracellular, N-terminus.
- Rat brain, rat skeletal muscle and mouse brain lysates, (1:200-1:1000).
Western blot analysis of rat brain (lanes 1 and 4), mouse brain (lanes 2 and 5) and rat skeletal muscle (lanes 3 and 6):1-3. Anti-SCN1B (NaVβ1) (extracellular) Antibody (#ASC-041), (1:400).
4-6. Anti-SCN1B (NaVβ1) (extracellular) Antibody, preincubated with SCN1B/Navβ1 (extracellular) Blocking Peptide (#BLP-SC041).
- Rat dorsal root ganglion (DRG).
- Differentiated rat PC12 cells (1:50).
Voltage-gated sodium channels (NaV) are essential for the generation of action potentials and for cell excitability.1 To date, nine NaV α subunits have been cloned and named NaV1.1-NaV1.9.2,3 Mammalian sodium channels are heterotrimers, composed of a central, pore-forming α subunit and two auxiliary β-subunits (NaV β-subunit).4
The NaV β-subunit gene family consists of four members: β1 (SCN1B), β2 (SCN2B), β3 (SCN3B), and β4 (SCN4B) having type I topology, containing an extracellular amino-terminus, a single transmembrane segment, and an intracellular carboxyl-terminus. They modulate channel gating, assembly, and cell surface expression in heterologous cell systems.5
NaV β-subunits are cell adhesion molecules of the Ig superfamily, which interact with extracellular matrix, transmembrane signaling, and cell adhesion molecules.5
In the adult central nervous system and heart, sodium channels are associate with β1-β4 subunits, whereas in adult skeletal muscle they are associate only with the β1 subunit.4,5 This association appears to be a late event in sodium channel biosynthesis.6
