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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 24 Oct 2014.

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
Sodium channel genes in pain-related disorders: phenotype-genotype associations and recommendations for clinical use.
New
Impact
Faber et al., New Haven, United States. In Lancet Neurol, 30 Nov 2014
Missense substitutions of SCN9A, the gene encoding sodium channel NaV1.7,
Effects of HIV-1 Tat on Enteric Neuropathogenesis.
New
Akbarali et al., Richmond, United States. In J Neurosci, 22 Nov 2014
Tat increased sodium channel isoforms Nav1.7 and Nav1.8 levels.
p.L1612P, a Novel Voltage-gated Sodium Channel Nav1.7 Mutation Inducing a Cold Sensitive Paroxysmal Extreme Pain Disorder.
New
Wider et al., Lausanne, Switzerland. In Anesthesiology, 03 Nov 2014
BACKGROUND:: Mutations in the SCN9A gene cause chronic pain and pain insensitivity syndromes.
Bioavailable pyrrolo-benzo-1,4-diazines as Nav1.7 sodium channel blockers for the treatment of pain.
New
Sorota et al., United States. In Bioorg Med Chem Lett, 19 Oct 2014
The optimization efforts allowed the identification of 33, a quinoline amide exhibiting potent Nav1.7 inhibitory activity and moderate selectivity over Nav1.5.
Channelopathies, painful neuropathy, and diabetes: which way does the causal arrow point?
Review
New
Waxman et al., Maastricht, Netherlands. In Trends Mol Med, Aug 2014
We suggest that mutations of sodium channel NaV1.7, which is present in both cell types, may increase susceptibility for development of diabetes via β cell injury and produce painful neuropathy via a distinct effect on DRG neurons.
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 neuropathies: the emerging role of sodium channelopathies.
New
Faber et al., Maastricht, Netherlands. In J Peripher Nerv Syst, Jun 2014
Voltage-gated sodium channels are responsible for the generation and conduction of action potentials in the peripheral nociceptive neuronal pathway where NaV 1.7, NaV 1.8, and NaV 1.9 sodium channels (encoded by SCN9A, SCN10A, and SCN11A) are preferentially expressed.
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.
Targeting voltage gated sodium channels NaV1.7, Na V1.8, and Na V1.9 for treatment of pathological cough.
Review
New
Undem et al., Baltimore, United States. In Lung, Feb 2014
Among the nine NaV subtypes (NaV1.1-NaV1.9), the afferent nerves involved in initiating cough, in common with nociceptive neurons in the somatosensory system, express mainly NaV1.7,
Ubiquitylation of voltage-gated sodium channels.
Review
New
Abriel et al., Bern, Switzerland. In Handb Exp Pharmacol, Dec 2013
Using two different mouse models, one with a specific knockout of Nedd4-2 in sensory neurons and another where Nedd4-2 was overexpressed with the use of viral vectors, it was demonstrated that the neuropathy-linked neuronal hyperexcitability was the result of Nav1.7 and Nav1.8 overexpression due to Nedd4-2 downregulation.
Altered sodium channel gating as molecular basis for pain: contribution of activation, inactivation, and resurgent currents.
Review
New
Waxman et al., Aachen, Germany. In Handb Exp Pharmacol, Dec 2013
Mutations in voltage-gated sodium channels, especially Nav1.7, can cause the genetic pain syndromes inherited erythromelalgia, small fiber neuropathy, paroxysmal extreme pain disorder, and chronic insensitivity to pain.
Congenital insensitivity to pain: a case report and review of the literature.
New
Grewal et al., Sharon, United States. In Case Report Neurol Med, Dec 2013
Congenital insensitivity to pain (CIP) is a rare autosomal recessive genetic disease caused by mutations in the SCN9A gene.
Voltage-gated sodium channel in grasshopper mice defends against bark scorpion toxin.
New
Impact
Zakon et al., Austin, United States. In Science, Nov 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.
Loss-of-function mutations in sodium channel Nav1.7 cause anosmia.
Impact
GeneRIF
Zufall et al., Homburg, Germany. In Nature, 2011
Na(v)1.7 is not only necessary for pain sensation but is also an essential requirement for odour perception in both mice and humans
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