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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
A model of breast cancer heterogeneity reveals vascular mimicry as a driver of metastasis.
Knott et al., New York City, United States. In Nature, 08 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.
Osteoarthritis dependent changes in antinociceptive action of Nav 1.7 and Nav1.8 sodium channel blockers: an in vivo electrophysiological study in the rat.
Dickenson et al., London, United Kingdom. In Neuroscience, 25 Apr 2015
Using a rat model of monosodium iodoacetate (MIA) induced osteoarthritis we used in vivo electrophysiology to assess the effects of the Nav1.7 and Nav 1.8 selective antagonists, ProTxII and A-803467 respectively, on the evoked activity of spinal dorsal horn neurons in response to electrical, mechanical and thermal stimuli applied to the peripheral receptive field.
The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy.
Waxman et al., New Haven, United States. In Neuromolecular Med, 20 Apr 2015
Gain-of-function variants of sodium channels Nav1.7 and Nav1.8 have recently been associated with painful small fiber neuropathy.
The serpin PN1 is a feedback regulator of FGF signaling in germ layer and primary axis formation.
Pera et al., Lund, Sweden. In Development, 15 Apr 2015
Here, we show that the serpin Protease nexin-1 (PN1) is transcriptionally activated by FGF signals, suppresses mesoderm and promotes head development in mRNA-injected embryos.
C-fiber recovery cycle supernormality depends on ion concentration and ion channel permeability.
Fransén et al., Stockholm, Sweden. In Biophys J, 10 Apr 2015
We further show that the supernormal phase results from a reduced potassium current Kdr as a result of accumulation of periaxonal potassium in concert with a reduced influx of sodium through Nav1.7 relative to Nav1.8 current.
Painful peripheral neuropathy and sodium channel mutations.
Waxman et al., Maastricht, Netherlands. In Neurosci Lett, Jan 2015
Voltage-gated sodium channels NaV1.7,
Differential response to sulfur nutrition of two common bean genotypes differing in storage protein composition.
Marsolais et al., London, Canada. In Front Plant Sci, Dec 2014
SARC1 and SMARC1N-PN1 are genetically related lines of common bean (dry bean, Phaseolus vulgaris) differing in seed storage protein composition.
Cellular hyper-excitability caused by mutations that alter the activation process of voltage-gated sodium channels.
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 channels and pain.
Cox et al., London, United Kingdom. In Handb Exp Pharmacol, Dec 2014
In this chapter, we focus on Nav1.7,
Identification of Novel Adipokines in the Joint. Differential Expression in Healthy and Osteoarthritis Tissues.
Gualillo et al., Santiago de Compostela, Spain. In Plos One, Dec 2014
Recently, novel adipokines such as SERPINE2, WISP2, GPNMB and ITIH5 have been identified in WAT.
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, 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.
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.
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.
Blechschmidt et al., Jena, Germany. In Glob Cardiol Sci Pract, 2013
Voltage-gated sodium channel in grasshopper mice defends against bark scorpion toxin.
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.
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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