Nav beta 3 Antibody, Clone N396/29: APC

NaVβ3 (encoded by SCN3B) is a regulatory subunit of voltage-gated sodium channels that modulates channel gating kinetics and neuronal excitability. Unlike other β subunits, NaVβ3 slows inactivation and promotes persistent sodium currents, which enhance synaptic input summation and increase neuronal responsiveness. This property may contribute to hyperexcitability in specific neuronal populations, a feature observed in epilepsy and neurodegenerative disorders. NaVβ3 also interacts with neurofascin, facilitating the localization and retention of sodium channels at the nodes of Ranvier in developing and mature myelinated axons. This interaction is essential for saltatory conduction and efficient neural signaling. Disruption of SCN3B has been linked to Brugada syndrome, highlighting its role in excitable tissue function. In the context of neurodegeneration, altered NaVβ3 expression or function may contribute to impaired action potential propagation, synaptic dysfunction, and neuronal vulnerability. Its role in modulating persistent sodium currents suggests a potential link to excitotoxicity and calcium overload, both of which are implicated in diseases such as ALS and Alzheimer’s disease. NaVβ3 thus represents a promising target for understanding and modulating neuronal excitability in neurodegenerative conditions.

A 1:100 dilution of SMC-490 was sufficient for detection of NavBeta3 in 20 µg of mouse brain lysate by ECL immunoblot analysis using Goat anti-mouse IgG:HRP as the secondary antibody.

1. Genes and mapped phenotypes. (n.d.). Retrieved March 26, 2015, from http://www.ncbi.nlm.nih.gov/gene/?term=Q9jK00 2. Qu Y., et al. (2001) Mol Cell Neurosci. 18(5): 570-580. 3. Ishikawa T., et al. (2013) Circ J. 77(4): 956-967.

1. Genes and mapped phenotypes. (n.d.) . Retrieved March 26, 2015, from http://www.ncbi.nlm.nih.gov/gene/?term=Q9jK00 2. Qu Y., et al. (2001) Mol Cell Neurosci. 18 (5) : 570-580. 3. Ishikawa T., et al. (2013) Circ J. 77 (4) : 956-967.