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Sodium channel, voltage-gated, type II, beta

forms a voltage gated sodium channel with alpha subunit; may modulate sodium channel expression in neurons [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: SCN1B, SCN5A, SCN3B, AGE, beta2
Papers on SCN2B
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.
Functions of miR-9 and miR-9* during Aging in SAMP8 Mice and Their Possible Mechanisms.
Peng et al., Beijing, China. In Zhongguo Yi Xue Ke Xue Yuan Xue Bao, Jun 2015
The predicted target genes of miR-9 were PSEN1,SCN2B,MAP3K3,and BACE1,and that of miR-9(*) was CDKn1c.
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.
Sodium Channel Voltage-Gated Beta 2 Plays a Vital Role in Brain Aging Associated with Synaptic Plasticity and Expression of COX5A and FGF-2.
Wang et al., Kunming, China. In Mol Neurobiol, Feb 2015
UNASSIGNED: The role of sodium channel voltage-gated beta 2 (SCN2B) in brain aging is largely unknown.
Comprehensive Genetic Characterization of a Spanish Brugada Syndrome Cohort.
Brugada et al., Girona, Spain. In Plos One, 2014
Regarding the sequencing of the minority genes, we discovered a potentially pathogenic variation in SCN2B that was described to alter sodium current, and one nonsense variant of unknown significance in RANGRF.
Influence of differentially expressed genes from suicide post-mortem study on personality traits as endophenotypes on healthy subjects and suicide attempters.
Rujescu et al., Brescia, Italy. In Eur Arch Psychiatry Clin Neurosci, 2014
Our primary aim was to investigate the potential modulation of several single-nucleotide polymorphisms (SNPs) of the same previously investigated genes (S100A13, EFEMP1, PCDHB5, PDGFRB, CDCA7L, SCN2B, PTPRR, MLC1 and ZFP36) on personality traits, as measured with the Temperament and Character Inventory (TCI), in a German sample composed of 287 healthy subjects (males: 123, 42.9 %; mean age: 45.2 ± 14.9 years) and in 111 psychiatric patients who attempted suicide (males: 43, 38.6 %; mean age: 39.2 ± 13.6 years).
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.
Case-control association study of polymorphisms in the voltage-gated sodium channel genes SCN1A, SCN2A, SCN3A, SCN1B, and SCN2B and epilepsy.
Kwan et al., Hong Kong, Hong Kong. In Hum Genet, 2014
High-frequency action potentials are mediated by voltage-gated sodium channels, composed of one large α subunit and two small β subunits, encoded mainly by SCN1A, SCN2A, SCN3A, SCN1B, and SCN2B genes in the brain.
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.
The effects of eslicarbazepine on persistent Na⁺ current and the role of the Na⁺ channel β subunits.
Uebachs et al., Bonn, Germany. In Epilepsy Res, 2014
To study the role of β subunits of the Na(+) channel we used a mouse line genetically lacking either the β1 or β2 subunit, encoded by the SCN1B or SCN2B gene, respectively.
Identification of beta-2 as a key cell adhesion molecule in PCa cell neurotropic behavior: a novel ex vivo and biophysical approach.
Sikes et al., Newark, United States. In Plos One, 2013
The beta-2 isoform (gene SCN2B) interacts with several neural CAMs, while interacting putatively with other prominent neural CAMs.
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.
A missense mutation in the sodium channel β2 subunit reveals SCN2B as a new candidate gene for Brugada syndrome.
Brugada et al., Girona, Spain. In Hum Mutat, 2013
In this work, we identified a novel missense mutation (p.Asp211Gly) in the sodium β2 subunit encoded by SCN2B, in a woman diagnosed with BrS.
Differential gene expression of cardiac ion channels in human dilated cardiomyopathy.
Rivera et al., Valencia, Spain. In Plos One, 2012
SCN2B was upregulated, while KCNJ5, KCNJ8, CLIC2, CLCN3, CACNB2, and CACNA1C were downregulated.
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 scn2b gene expression in mouse dorsal raphe nucleus
Loss of Na+ channel beta2 subunits is neuroprotective in a mouse model of multiple sclerosis.
Isom et al., Ann Arbor, United States. In Mol Cell Neurosci, 2009
Data suggest that loss of sodium channel beta2 subunit is neuroprotective in experimental allergic encephalomyelitis by prevention of Na+ channel up-regulation in response to demyelination.
Upregulation of the voltage-gated sodium channel beta2 subunit in neuropathic pain models: characterization of expression in injured and non-injured primary sensory neurons.
Decosterd et al., Lausanne, Switzerland. In J Neurosci, 2005
Increased beta2 subunit expression in sensory neurons after nerve injury is functionally significant. Development of mechanical allodynia-like behavior in the SNI model is attenuated in beta2 subunit null mutant mice.
Presenilin/gamma-secretase-mediated cleavage of the voltage-gated sodium channel beta2-subunit regulates cell adhesion and migration.
Kovacs et al., United States. In J Biol Chem, 2005
beta2 is a PS/gamma-secretase substrate, gamma-secretase mediated cleavage of beta2-C-terminal fragment is required for cell-cell adhesion and migration of beta2-expressing cells
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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