SCN3B Membrane Protein Introduction

Introduction of SCN3B

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
Gene Name	SCN3B
Aliases	ATFB16, BRGDA7, HSA243396, SCNB3
Organism	Homo sapiens (Human)
UniProt ID	Q9NY72
Transmembrane Times	1
Length (aa)	215
Sequence	MPAFNRLFPLASLVLIYWVSVCFPVCVEVPSETEAVQGNPMKLRCISCMKREEVEATTVVEWFYRPEGGKDFLIYEYRNGHQEVESPFQGRLQWNGSKDLQDVSITVLNVTLNDSGLYTCNVSREFEFEAHRPFVKTTRLIPLRVTEEAGEDFTSVVSEIMMYILLVFLTLWLLIEMIYCYRKVSKAEEAAQENASDYLAIPSENKENSAVPVEE

Function of SCN3B Membrane Protein

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))

Application of SCN3B Membrane Protein in Literature

Ishikawa T., et al. Novel SCN3B mutation associated with Brugada syndrome affects intracellular trafficking and function of Nav1.5. Circulation Journal. 2013, 77(4):959-67. PubMed ID: 23257389

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.
Zhao Y., et al. Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells. BMC Cardiovasc Disord. 2016, 16:1. PubMed ID: 26728597

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.
Okata S., et al. Embryonic type Na⁺ channel β-subunit, SCN3B masks the disease phenotype of Brugada syndrome. Scientific Report. 2016, 6:34198. PubMed ID: 27677334

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.
Olesen M.S., et al. Mutations in sodium channel β-subunit SCN3B are associated with early-onset lone atrial fibrillation. Cardiovascular Research. 2011, 89(4):786-93. PubMed ID: 21051419

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.
Hakim P., et al. Scn3b knockout mice exhibit abnormal sino-atrial and cardiac conduction properties. Acta physiologica (Oxford, England). 2010, 198(1):47-59. PubMed ID: 19796257

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.

SCN3B Preparation Options

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Reference

Campuzano O, et al. (2015). Genetics of channelopathies associated with sudden cardiac death. Global Cardiology Science and Practice. 3: 39.

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