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Sodium channel, voltage-gated, type III, beta

SCN3B, voltage-gated sodium channel beta3 subunit
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] (from NCBI)
Top mentioned proteins: SCN5A, SCN1B, SCN2B, CAN, Cav1.2
Papers on SCN3B
Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells.
Tu et al., Wuhan, China. In Bmc Cardiovasc Disord, Dec 2015
METHODS: In the present study, we observed the effect of IL-2 by qRT-PCR on the transcription of ion channel genes including SCN2A, SCN3A, SCN4A, SCN5A, SCN9A, SCN10A, SCN1B, SCN2B, SCN3B, KCNN1, KCNJ5, KCNE1, KCNE2, KCNE3, KCND3, KCNQ1, KCNA5, KCNH2 and CACNA1C.
Identification of novel gene and pathway targets for human epilepsy treatment.
Wei et al., Jilin, China. In Biol Res, Dec 2015
In up-co-expression module, SCN3B (sodium channel, voltage gated, type III beta subunit) was enriched in GO:0006814 ~ sodium ion transport.
The role of the sodium current complex in a nonreferred nationwide cohort of sudden infant death syndrome.
Jespersen et al., Copenhagen, Denmark. In Heart Rhythm, Jun 2015
In total, 66 non-referred SIDS cases born in Denmark in the period of 2000-2006 were screened for genetic variants in the 8 major genes involved in the regulation of the Nav1.5 channel complex: SCN5A, SCN1B, SCN2B, SCN3B, SCN4B, GPD1L, SNTA1, and CAV3.
Modulation of microRNA-375 expression alters voltage-gated Na(+) channel properties and exocytosis in insulin-secreting cells.
Eliasson et al., Malmö, Sweden. In Acta Physiol (oxf), Apr 2015
Potential targets differed among species and expression of suggested targets Scn3a and Scn3b in INS-1 832/13 cells was only slightly moderated by miR-375.
Genetic Analysis of Arrhythmogenic Diseases in the Era of NGS: The Complexity of Clinical Decision-Making in Brugada Syndrome.
Brugada et al., Girona, Spain. In Plos One, 2014
Twenty-eight genes were resequenced: AKAP9, ANK2, CACNA1C, CACNB2, CASQ2, CAV3, DSC2, DSG2, DSP, GPD1L, HCN4, JUP, KCNE1, KCNE2, KCNE3, KCNH2, KCNJ2, KCNJ5, KCNQ1, NOS1AP, PKP2, RYR2, SCN1B, SCN3B, SCN4B, SCN5A, SNTA1, and TMEM43.
A missense mutation in the sodium channel β1b subunit reveals SCN1B as a susceptibility gene underlying long QT syndrome.
Brugada et al., Girona, Spain. In Heart Rhythm, 2014
METHODS: We screened for mutations in the genes encoding the 5 sodium β subunits (SCN1B isoforms a and b, SCN2B, SCN3B, and SCN4B) from 30 nonrelated patients who were clinically diagnosed with LQTS without mutations in common LQTS-related genes.
Is sudden unexplained nocturnal death syndrome in Southern China a cardiac sodium channel dysfunction disorder?
Cheng et al., Guangzhou, China. In Forensic Sci Int, 2014
Genomic DNA extracted from the blood samples of 123 medico-legal autopsy-negative SUNDS cases and 104 sex-, age- and ethnic-matched controls from Southern China underwent comprehensive amino acid coding region mutational analysis for the BrS associated genes SCN5A, SCN1B, SCN2B, SCN3B, SCN4B, MOG1, and GPD1-L using PCR and direct sequencing.
Transcription profiles of the ductus arteriosus in Brown-Norway rats with irregular elastic fiber formation.
Minamisawa et al., In Circ J, 2013
Among these genes, 8 (Tbx20, Scn3b, Stac, Sphkap, Trpm8, Rup2, Slc37a2, and RGD1561216) are located in chromosomes 8 and 9. Interestingly, it was also suggested that the significant decrease in the expression levels of the PGE2-specfic receptor, EP4, plays a critical role in elastogenesis in the DA.
[SCN5A mutation in patients with Brugada electrocardiographic pattern induced by fever].
Hong et al., Nanchang, China. In Zhonghua Xin Xue Guan Bing Za Zhi, 2013
OBJECTIVE: To explore the relationship between SCN5A, SCN1b, SCN3b and GPD1L genotypes and the risk of malignant arrhythmia in patients with Brugada electrocardiographic pattern induced by fever.
Mutations of the SCN4B-encoded sodium channel β4 subunit in familial atrial fibrillation.
Yang et al., Shanghai, China. In Int J Mol Med, 2013
Mutations in the cardiac sodium channel α, β1, β2 and β3 subunit genes (SCN5A, SCN1B, SCN2B and SCN3B) have been associated with AF, which suggests that mutations in the sodium channel β4 subunit gene, SCN4B, are also involved in the pathogenesis of AF.
Modulation of mononuclear phagocyte inflammatory response by liposome-encapsulated voltage gated sodium channel inhibitor ameliorates myocardial ischemia/reperfusion injury in rats.
Li et al., Tianjin, China. In Plos One, 2012
NaVX, Scn1b, Scn3b and Scn4b) and β subunits were expressed at mRNA level, and PHT could suppress lipopolysaccharide induced M1 polarization (decreased TNF-α and CCL5 expression) and facilitate interleukin-4 induced M2 polarization (increased Arg1 and TGF-β1 expression).
Patterned expression of ion channel genes in mouse dorsal raphe nucleus determined with the Allen Mouse Brain Atlas.
Commons et al., Boston, United States. In Brain Res, 2012
This study demonistrated that scn3b gene expression in mouse dorsal raphe nucleus
Genetic and clinical aspects of Brugada syndrome: an update.
Cervellin et al., Parma, Italy. In Adv Clin Chem, 2011
Accordingly, eight types of BS (from BS1 to BS8) have already been described, involving mutations in SCN5A, GPD1-L, CACNA1c, CACNB2b, SCN1B, KCNE3, SCN3B, and HCN4 genes.
"Benign" early repolarization versus malignant early abnormalities: clinical-electrocardiographic distinction and genetic basis.
Baranchuk et al., Santo André, Brazil. In Cardiol J, 2011
The inherited-familial forms are not frequent in IVF; however mutations were identified in the genes KCNJ8, DPP6, SCN5A, SCN3B, CACNA1C, CACNB2, and CACNA2D1.
Increased expression of the beta3 subunit of voltage-gated Na+ channels in the spinal cord of the SOD1G93A mouse.
Longone et al., Roma, Italy. In Mol Cell Neurosci, 2011
These data suggest that the SOD1G93A mutation results in increased expression of the beta3 subunit of voltage-gated Na+ channels in the spinal cord..
Mutations in sodium channel β-subunit SCN3B are associated with early-onset lone atrial fibrillation.
Svendsen et al., Copenhagen, Denmark. In Cardiovasc Res, 2011
three mutations in SCN3B were investigated electrophysiologically and all led to loss of function in the sodium current, supporting the hypothesis that decreased sodium current enhances atrial fibrillation susceptibility
The sodium channel {beta}3-subunit induces multiphasic gating in NaV1.3 and affects fast inactivation via distinct intracellular regions.
Jackson et al., Cambridge, United Kingdom. In J Biol Chem, 2010
The sodium channel {beta}3-subunit induces multiphasic gating in NaV1.3 and affects fast inactivation via distinct intracellular regions.
Functional dominant-negative mutation of sodium channel subunit gene SCN3B associated with atrial fibrillation in a Chinese GeneID population.
Wang et al., Wuhan, China. In Biochem Biophys Res Commun, 2010
This study identifies the first atrial fibrillation(AF) -associated mutation in SCN3B, and suggests that mutations in SCN3B may be a new pathogenic cause of AF.
The genetic basis of Brugada syndrome: a mutation update.
Christiansen et al., Copenhagen, Denmark. In Hum Mutat, 2009
ion channel; SCN1B and SCN3B, which, in the heart, encodes beta-subunits of the Na(v)1.5 sodium ion channel, and KCNE3, which encodes the ancillary inhibitory beta-subunit of several potassium channels including the Kv4.3 ion channel conducting the repolarizing potassium I(to) current.
Brugada Syndrome
Hong et al., Seattle, United States. In Unknown Journal, 2005
Pathogenic variants in 16 genes have been associated with Brugada syndrome: SCN5A, SCN1B, SCN2B, SCN3B, GPD1L, CACNA1C, CACNB2, CACNA2D1, KCND3, KCNE3, KCNE1L (KCNE5), KCNJ8, HCN4, RANGRF, SLMAP, and TRPM4.
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