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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 17 May 2015.

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

PN1, Nav1.7, Gdn, SCN9A, SERPINE2
This gene encodes a voltage-gated sodium channel which plays a significant role in nociception signaling. Mutations in this gene have been associated with primary erythermalgia, channelopathy-associated insensitivity to pain, and paroxysmal extreme pain disorder. [provided by RefSeq, Aug 2009] (from NCBI)
Top mentioned proteins: CAN, HAD, ACID, V1a, Plasminogen
Papers on PN1
Identification and Characterization of ProTx-III [μ-TRTX-Tp1a], A New Voltage-Gated Sodium Channel Inhibitor from Venom of the Tarantula Thrixopelma Pruriens.
New
Lewis et al., Australia. In Mol Pharmacol, 15 Jun 2015
NaV1.7 inhibition was diminished (IC50 11.5 nM), and the association rate decreased, for the C-terminal acid form of Tp1a compared to the native amidated form (IC50 2.1 nM), suggesting that the peptide C-terminus contributes to its interaction with hNaV1.7.
Sodium channel NaV1.7 in vascular myocytes, endothelium, and innervating axons in human skin.
New
Waxman et al., United States. In Mol Pain, 09 Jun 2015
Two autosomal dominant disorders characterized by episodes of severe pain, inherited erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD) have been directly linked to mutations that enhance the function of sodium channel NaV1.7.
Modification of N staging systems for penile cancer: a more precise prediction of prognosis.
New
Han et al., Guangzhou, China. In Br J Cancer, 05 Jun 2015
RESULTS: According to the 7th edition of the pathological N classification, the 3-year disease-specific survival (DSS) rates for patients with pN1, pN2, and pN3 disease are 89.6%,
Voltage-Gated Sodium Channels: Structure, Function, Pharmacology and Clinical Indications.
New
Kraus et al., In J Med Chem, 30 May 2015
Nav1.7 channels in particular have received much attention recently because of strong genetic validation of their involvement in nociception.
A model of breast cancer heterogeneity reveals vascular mimicry as a driver of metastasis.
New
Impact
Knott et al., New York City, United States. In Nature, 16 May 2015
Those clones that efficiently enter the vasculature express two secreted proteins, Serpine2 and Slpi, which were necessary and sufficient to program these cells for vascular mimicry.
Metastatic lymph node ratio successfully predicts prognosis in western gastric cancer patients.
Review
New
Dissanaike et al., United States. In Surg Oncol, 24 Apr 2015
AJCC 7th edition nodal staging (N0: 0, N1:1-2, N2:3-6, N3:≥7 positive lymph nodes) and LNR positive nodal staging (PN0: 0%, PN1: 1-20%, PN2: 21-50%, PN3: 51-100% of examined nodes positive) were compared as respects seven year survivorship.
Painful peripheral neuropathy and sodium channel mutations.
Review
New
Waxman et al., Maastricht, Netherlands. In Neurosci Lett, Jan 2015
Voltage-gated sodium channels NaV1.7,
Mapping quantitative trait loci for yield-related traits in soybean (Glycine max L.).
New
Srinives et al., Nakhon Pathom, Thailand. In Breed Sci, Dec 2014
However, four novel QTLs including SF1, SF2 and SF3 on linkage groups L and N for seed filling period and PN1 on linkage group D1b for pod number were identified in the present study.
Cellular hyper-excitability caused by mutations that alter the activation process of voltage-gated sodium channels.
Review
New
Abriel et al., Taza, Morocco. In Front Physiol, Dec 2014
The p.I141V mutation in SCN4A and SCN5A, as well as its homologous p.I136V mutation in SCN9A, are interesting examples of mutations that have been linked to inherited hyperexcitability myotonia, exercise-induced polymorphic ventricular arrhythmias and erythromelalgia, respectively.
Sodium channel genes in pain-related disorders: phenotype-genotype associations and recommendations for clinical use.
Review
New
Impact
Faber et al., New Haven, United States. In Lancet Neurol, Nov 2014
Missense substitutions of SCN9A, the gene encoding sodium channel NaV1.7,
A monoclonal antibody that targets a NaV1.7 channel voltage sensor for pain and itch relief.
New
Impact
Lee et al., Durham, United States. In Cell, Jul 2014
Here, we present a monoclonal antibody that targets the voltage-sensor paddle of NaV1.7, the subtype critical for pain sensation.
Painful and painless channelopathies.
Review
New
Impact
Woods et al., Cambridge, United Kingdom. In Lancet Neurol, Jun 2014
For example, the voltage-gated sodium ion channel Nav1.7 is expressed selectively in sensory and autonomic neurons; inactivating mutations in SCN9A, which encodes Nav1.7, result in congenital insensitivity to pain, whereas gain-of-function mutations in this gene produce distinct pain syndromes such as inherited erythromelalgia, paroxysmal extreme pain disorder, and small-fibre neuropathy.
Voltage-gated sodium channels in the mammalian heart.
Review
Blechschmidt et al., Jena, Germany. In Glob Cardiol Sci Pract, 2013
Nav1.7).
Voltage-gated sodium channel in grasshopper mice defends against bark scorpion toxin.
Impact
Zakon et al., Austin, United States. In Science, 2013
Bark scorpion venom induces pain in many mammals (house mice, rats, humans) by activating the voltage-gated Na(+) channel Nav1.7, but has no effect on Nav1.8.
Voltage-gated sodium channel activity promotes prostate cancer metastasis in vivo.
GeneRIF
Djamgoz et al., İstanbul, Turkey. In Cancer Lett, 2012
the involvement of functional voltage-gated sodium channels expression as a potentiating factor in metastatic prostate cancer has been confirmed in vivo for the first time
Sodium channel Na(v)1.7 is essential for lowering heat pain threshold after burn injury.
GeneRIF
Waxman et al., New Haven, United States. In J Neurosci, 2012
The results of this study suggested that Sodium channel Na(v)1.7 is essential for lowering heat pain threshold after burn injury.
Crystal structures of protease nexin-1 in complex with heparin and thrombin suggest a 2-step recognition mechanism.
GeneRIF
Huntington et al., Cambridge, United Kingdom. In Blood, 2012
crystal structures of PN1 in complex with heparin and catalytically inert thrombin suggest a unique 2-step mechanism of thrombin recognition involving rapid electrostatics-driven association
Nav1.7-related small fiber neuropathy: impaired slow-inactivation and DRG neuron hyperexcitability.
GeneRIF
Waxman et al., New Haven, United States. In Neurology, 2012
The I739V Nav1.7 variant in a patient with biopsy-confirmed idiopathic small fiber neuropathy impairs slow-inactivation within dorsal root ganglion neurons and increases their excitability.
Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons.
GeneRIF
Wood et al., London, United Kingdom. In Nat Commun, 2011
Deleting SCN9A in both sensory and sympathetic neurons abolishes pain sensations.
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