SCN3B Antibody – Rabbit Polyclonal

Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel beta subunit gene family, and influences the inactivation kinetics of the sodium channel. Two alternatively spliced variants, encoding the same protein, have been identified. [provided by RefSeq, Jul 2008]

SCN3B: Modulates channel gating kinetics. Causes unique persistent sodium currents. Inactivates the sodium channel opening more slowly than the subunit beta-1. Its association with neurofascin may target the sodium channels to the nodes of Ranvier of developing axons and retain these channels at the nodes in mature myelinated axons. Defects in SCN3B are the cause of Brugada syndrome type 7 (BRGDA7). A tachyarrhythmia characterized by right bundle branch block and ST segment elevation on an electrocardiogram (ECG). It can cause the ventricles to beat so fast that the blood is prevented from circulating efficiently in the body. When this situation occurs (called ventricular fibrillation), the individual will faint and may die in a few minutes if the heart is not reset. Belongs to the sodium channel auxiliary subunit SCN3B (TC 8.A.17) family.

Protein type: Membrane protein, integral; Channel, sodium

Chromosomal Location of Human Ortholog: 11q23.3

Cellular Component: voltage-gated sodium channel complex; plasma membrane; integral to membrane; Z disc

Molecular Function: sodium channel regulator activity; voltage-gated sodium channel activity

Biological Process: membrane depolarization; nervous system development; sodium ion transport; positive regulation of heart rate; sensory perception of pain; cardiac muscle contraction

Disease: Brugada Syndrome 7