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Sodium channel, voltage-gated, type III, alpha subunit

Nav1.3, SCN3A
Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with 24 transmembrane domains 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 alpha subunit gene family, and is found in a cluster of five alpha subunit genes on chromosome 2. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PN1, Omi, SCN5A, CAN, HAD
Papers on Nav1.3
Benzonatate inhibition of voltage-gated sodium currents.
Johnson et al., Louisville, United States. In Neuropharmacology, Feb 2016
We used whole cell voltage clamp recording to test the effects of benzonatate on voltage-gated sodium (Na(+)) currents in two murine cell lines, catecholamine A differentiated (CAD) cells, which express primarily Nav1.7, and N1E-115, which express primarily Nav1.3.
Differential effects of the recombinant toxin PnTx4(5-5) from the spider Phoneutria nigriventer on mammalian and insect sodium channels.
de Lima et al., Belo Horizonte, Brazil. In Biochimie, Jan 2016
Interestingly, the toxin also inhibited sodium current on all the mammalian channels tested, with the higher current inhibition on Nav1.3 (38.43 ± 8.04%, IC50 = 1.5 μM).
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.
An update on transcriptional and post-translational regulation of brain voltage-gated sodium channels.
Beltran-Alvarez et al., Kingston upon Hull, United Kingdom. In Amino Acids, Nov 2015
SCN3A (NaV1.3)
Isobaric Tags for Relative and Absolute Quantitation-Based Proteomic Analysis of Patent and Constricted Ductus Arteriosus Tissues Confirms the Systemic Regulation of Ductus Arteriosus Closure.
Zhang et al., Shanghai, China. In J Cardiovasc Pharmacol, Aug 2015
Of 132 proteins, voltage-gated sodium channel 1.3 (SCN3A), myosin 1d (Myo1d), Rho GTPase activating protein 26 (ARHGAP26), and retinitis pigmentosa 1 (RP1) were selected for validation by Western blot and quantitative real-time polymerase chain reaction analyses.
Alkaloids from Veratrum taliense Exert Cardiovascular Toxic Effects via Cardiac Sodium Channel Subtype 1.5.
Luo et al., Nanjing, China. In Toxins (basel), 2014
A pathophysiological study indicated that these VAs blocked sodium channels NaV1.3-1.5 and exhibited the strongest ability to inhibit NaV1.5, which is specifically expressed in cardiac tissue and plays an essential role in cardiac physiological function.
Sodium channels and pain.
Cox et al., London, United Kingdom. In Handb Exp Pharmacol, 2014
Nav1.8, Nav1.9 and Nav1.3 and describe the insights gained from the detailed analyses of global and conditional transgenic Nav knockout mice in terms of pain behaviour.
Voltage-Gated Sodium Channels as Therapeutic Targets for Treatment of Painful Diabetic Neuropathy.
Sharma et al., India. In Mini Rev Med Chem, 2014
Peripheral nociceptive neurons express variety of sodium channel isoforms particularly Nav1.3,
Tumor necrosis factor-α enhances voltage-gated Na⁺ currents in primary culture of mouse cortical neurons.
Li et al., Shantou, China. In J Neuroinflammation, 2014
Expression of Nav1.1, Nav1.2, Nav1.3, and Nav1.6 were examined at both the mRNA and protein levels, prior to and after TNF-α exposure.
Virus-Mediated Knockdown of Nav1.3 in Dorsal Root Ganglia of STZ-Induced Diabetic Rats Alleviates Tactile Allodynia.
Waxman et al., West Haven, United States. In Mol Med, 2014
Voltage-gated sodium channel Nav1.3 produces tetrodotoxin-sensitive sodium currents with rapid repriming kinetics and has been shown to contribute to neuronal hyperexcitability and ectopic firing in injured neurons.
The Scorpion Toxin Tf2 from Tityus fasciolatus Promotes Nav1.3 Opening.
Schwartz et al., Brasília, Brazil. In Plos One, 2014
We found that Tf2 selectively activates human (h)Nav1.3, a neuronal voltage-gated sodium (Nav) subtype implicated in epilepsy and nociception.
Structure and function of μ-conotoxins, peptide-based sodium channel blockers with analgesic activity.
Norton et al., Australia. In Future Med Chem, 2014
NaV1.3 or NaV1.7).
Voltage-gated sodium channels in the mammalian heart.
Blechschmidt et al., Jena, Germany. In Glob Cardiol Sci Pract, 2013
Nav1.3, Nav1.6), in the skeletal muscle (Nav1.4),
Noncanonical roles of voltage-gated sodium channels.
Waxman et al., New Haven, United States. In Neuron, 2013
Sodium channels Nav1.1-Nav1.3 and Nav1.6-Nav1.9
Upregulated expression of voltage-gated sodium channel Nav1.3 in cortical lesions of patients with focal cortical dysplasia type IIb.
Yang et al., Chongqing, China. In Neuroreport, 2012
Upregulation of Nav1.3 protein and a specific cellular distribution of Nav1.3 proteins in focal cortical dysplasia type IIb(FCDIIb) lesion tissue samples suggest that Nav1.3 may be involved in the generation of epileptic activity in FCDIIb.
Promoter analysis of mouse Scn3a gene and regulation of the promoter activity by GC box and CpG methylation.
Long et al., Guangzhou, China. In J Mol Neurosci, 2011
These results suggest that the GC box and CpG methylation might play important roles in regulating mouse Scn3a gene expression.
Inhibition of NF-kappaB prevents mechanical allodynia induced by spinal ventral root transection and suppresses the re-expression of Nav1.3 in DRG neurons in vivo and in vitro.
Liu et al., Guangzhou, China. In Brain Res, 2011
injury to ventral root might lead to neuropathic pain and the re-expression of Nav1.3 in primary sensory neurons by activation of NF-kappaB
A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons.
Waxman et al., New Haven, United States. In Exp Neurol, 2010
Data provide a pathophysiological basis for the pathogenicity of the first epilepsy-linked mutation within Na(V)1.3 channels and hippocampal neurons.
Array-CGH detection of a de novo 2.8 Mb deletion in 2q24.2-->q24.3 in a girl with autistic features and developmental delay.
Wang et al., Taipei, Taiwan. In Eur J Med Genet, 2010
Deletions in SCN3A gene is associated with autistic features and developmental delay.
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