Sodium channel subunit beta-3 (SCN3B) is encoded by SCN3B gene, which is located on the chromosome11q24.1. The molecular mass of SCN3B is 24 kDa. SCN3B is non-covalently associated with alpha subunit to form voltage-sensitive sodium channel which usually is a transmembrane glycoprotein complex. SCN3B regulates sodium channel alpha subunit and influences the inactivation kinetics of the sodium channel.
|Basic Information of SCN3B|
|Protein Name||Sodium channel subunit beta-3|
|Aliases||ATFB16, BRGDA7, HSA243396, SCNB3|
|Organism||Homo sapiens (Human)|
SCN3B modulates channel gating kinetics and causes unique persistent sodium currents. SCN3B inactivates the sodium channel opening more slowly than the subunit beta-1. Its association with NFASC may target the sodium channels in the nodes of Ranvier in developing axons and retain these channels at the nodes in mature myelinated axons. Diseases associated with SCN3B include Brugada syndrome 7 and Brugada syndrome. SCN3B is associated with cardiac conduction and L1CAM interactions pathways. Gene Ontology (GO) annotations related to this gene include ion channel binding and voltage-gated sodium channel activity. An important paralog of this gene is SCN1B.
Fig.1 Diagram of overlapping genes associated with main cardiac channelopathies. (Campuzano, 2015))
This article finds that the Val110Ile mutation of SCN3B is a relatively common cause of SCN5A-negative BrS leading to a reduced sodium current in Japan.
This article suggests that IL-2 may play a role in the arrhythmia by regulating SCN3B/scn3b expression and increasing sodium current in myocardial cells.
This article suggests that LQTS3/BrS iPSC-derived cardiomyocytes recapitulate the disease phenotype of LQTS3, which is frequently associated with sudden death in the young, but not that of BrS, which is frequently associated with sudden death in adults.
This article reveals that three mutations in SCN3B lead to loss of function in the sodium current, supporting the hypothesis that decreased sodium current enhances AF susceptibility.
This article suggests that a deficiency in Scn3b results in significant atrial electrophysiological and intracardiac conduction abnormalities, complementing the changes in ventricular electrophysiology reported on an earlier occasion.
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