SCN3B Protein, Human (HEK293, Fc)

The SCN3B protein critically affects sodium channel dynamics, inducing unique sustained currents and slower inactivation rates compared to beta-1. Its interaction with NFASC is shown to guide sodium channels to the nodes of Ranvier during axonal development and retain them in mature myelinated axons. SCN3B Protein, Human (HEK293, Fc) is the recombinant human-derived SCN3B protein, expressed by HEK293 , with C-hFc labeled tag. The total length of SCN3B Protein, Human (HEK293, Fc) is 159 a.a., with molecular weight of 50-55 kDa.

SCN3B protein plays a crucial role in modulating the kinetics of channel gating, resulting in distinctive persistent sodium currents. In comparison to the beta-1 subunit, SCN3B induces a slower inactivation of sodium channels, influencing their opening dynamics. The interaction of SCN3B with NFASC suggests its potential involvement in directing sodium channels to the nodes of Ranvier during axonal development and retaining them at these nodes in mature myelinated axons. The voltage-sensitive sodium channel, comprising an ion-conducting pore-forming alpha-subunit, is intricately regulated by beta-1, beta-2, beta-3, and/or beta-4 subunits. Notably, beta-1 and beta-3 associate non-covalently with alpha, while beta-2 and beta-4 form covalent bonds through disulfide linkages, contributing to the functional complexity of the sodium channel complex.

Human

HEK293

C-hFc

Q9NY72 (M1-E159)

55800  [NCBI]

50-55 kDa

Greater than 95% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.