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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
Catalytic asymmetric hetero-Diels-Alder reactions of enones with isatins to access functionalized spirooxindole tetrahydropyrans: scope, derivatization, and discovery of bioactives.
Tanaka et al., Okinawa, Japan. In Org Biomol Chem, Feb 2016
From these synthesized compounds, an inhibitor of human ion channel Nav1.7 with μM-level activity was identified, indicating that the developed reaction methods are useful for providing molecules for the discovery of new biofunctional molecules.
Osteoarthritis year in review 2015: biology.
Malfait, Chicago, United States. In Osteoarthritis Cartilage, Jan 2016
Finally, a small selection of novel analgesic targets in the periphery is briefly discussed, including calcitonin gene-related peptide and the neuronal sodium voltage-gated channels, Nav1.7 and Nav1.8.
Genotypic Analysis of SCN9A for Prediction of Postoperative Pain in Female Patients Undergoing Gynecological Laparoscopic Surgery.
Zhang et al., Wuhan, China. In Pain Physician, Jan 2016
BACKGROUND: The SCN9A gene product is a critical component in human pain perception.
Structural basis of Nav1.7 inhibition by an isoform-selective small-molecule antagonist.
Payandeh et al., San Francisco, United States. In Science, Jan 2016
Targeting the human Nav1.7 channel involved in pain perception, we present a protein-engineering strategy that has allowed us to determine crystal structures of a novel receptor site in complex with isoform-selective antagonists.
Analgesic drug delivery via recombinant tissue plasminogen activator and microRNA-183-triggered opening of the blood-nerve barrier.
Rittner et al., Würzburg, Germany. In Biomaterials, Jan 2016
This facilitated an increase of nociceptive thresholds after local application of hydrophilic opioids or the voltage gated sodium channel blocker (NaV1.7)
Novel sodium channel antagonists in the treatment of neuropathic pain.
Zuliani et al., Parma, Italy. In Expert Opin Investig Drugs, Jan 2016
At this time, researchers have identified and characterized selective compounds against NaV1.7 or NaV1.8 voltage-gated sodium channels but only time will tell if they reach the market.
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.
New Mendelian Disorders of Painlessness.
Woods et al., Cambridge, United Kingdom. In Trends Neurosci, Nov 2015
Drugs targeting two previously discovered painlessness genes, NGF and SCN9A, are currently in late-stage clinical trials; thus, characterization of these new painlessness genes has significant potential for the generation of new classes of analgesics.
The effect of cell disruption techniques and chaotropic agents on the downstream purification process of mecasermin produced as inclusion body in E. coli.
Mofid et al., Eşfahān, Iran. In Res Pharm Sci, Nov 2015
We also investigated the solubilization profile of the top-notch IB in 6 M guanidine hydrochloride (Gdn-HCl) and 8 M urea at different pH ranges.
A model of breast cancer heterogeneity reveals vascular mimicry as a driver of metastasis.
Knott et al., New York City, United States. In Nature, 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.
Post-translational modifications of voltage-gated sodium channels in chronic pain syndromes.
Decosterd et al., Boston, United States. In Front Pharmacol, 2014
Studying the mutations associated with the increase or absence of pain sensitivity in humans, as well as other expression studies, have highlighted Nav1.7,
Sodium channel genes in pain-related disorders: phenotype-genotype associations and recommendations for clinical use.
Faber et al., New Haven, United States. In Lancet Neurol, 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.
Lee et al., Durham, United States. In Cell, 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.
Woods et al., Cambridge, United Kingdom. In Lancet Neurol, 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 channel activity promotes prostate cancer metastasis in vivo.
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.
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.
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.
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.
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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