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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
Copper-catalysed cross-coupling of arylzirconium reagents with aryl and heteroaryl iodides.
Giri et al., Albuquerque, United States. In Chem Commun (camb), 19 Mar 2015
Mechanistic studies with a Cp2ZrAr2 complex revealed that Cp2Zr(Ar)(Cl) is the reactive species that undergoes transmetalation with (PN-1)CuI.
Changes of voltage-gated sodium channels in sensory nerve regeneration and neuropathic pain models.
Navarro et al., Barcelona, Spain. In Restor Neurol Neurosci, 19 Mar 2015
Results: Both nerve injuries induced similar alterations in the VGSCs expression at 7 dpi, with upregulation of Nav1.3, and downregulation of Nav1.7,
Engineering Potent and Selective Analogs of GpTx-1, a Tarantula Venom Peptide Antagonist of the NaV1.7 Sodium Channel.
Miranda et al., In J Med Chem, 06 Mar 2015
UNASSIGNED: NaV1.7 is a voltage-gated sodium ion channel implicated by human genetic evidence as a therapeutic target for the treatment of pain.
Experimental and computational evidence for an essential role of NaV1.6 in spike initiation at stretch-sensitive colorectal afferent endings.
Gebhart et al., Baltimore, United States. In J Neurophysiol, 04 Mar 2015
Immunohistological staining and western blots revealed the presence of NaV1.6 and NaV1.7 channels at sensory neuronal endings in mouse colorectal tissue.
Overexpression of Plasminogen Activator Inhibitor-1 in Advanced Gastric Cancer with Aggressive Lymph Node Metastasis.
Yang et al., Seoul, South Korea. In Cancer Res Treat, 02 Mar 2015
Results: CFTR, LAMC2, SERPINE2, F2R, MMP7, FN1, TIMP1, plasminogen activator inhibitor-1 (PAI-1), ITGB8, SDS, and TMPRSS4 were commonly up-regulated over 2-fold in highN.
Protease nexin 1 induces apoptosis of prostate tumor cells through inhibition of X-chromosome-linked inhibitor of apoptosis protein.
Xu et al., Oxford, United Kingdom. In Oncotarget, 19 Feb 2015
UNASSIGNED: Protease nexin 1 (PN1) is an endogenous serine protease inhibitor (SERPIN), expressed at high levels in the prostate, and capable of inhibiting the proliferation of prostate cancer cells.
Painful peripheral neuropathy and sodium channel mutations.
Waxman et al., Maastricht, Netherlands. In Neurosci Lett, Jan 2015
Voltage-gated sodium channels 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, 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.
Ubiquitylation of voltage-gated sodium channels.
Abriel et al., Bern, Switzerland. In Handb Exp Pharmacol, 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.
Waxman et al., Aachen, Germany. In Handb Exp Pharmacol, 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.
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., ─░stanbul, 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.
Nav1.7 protein and mRNA expression in the dorsal root ganglia of rats with chronic neuropathic pain.
Zang et al., Zhengzhou, China. In Neural Regen Res, 2012
The results of immunohistochemistry, western blot assays and reverse transcription-PCR showed that Nav1.7 protein and mRNA expression was significantly increased in the injured dorsal root ganglia.
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.
Loss-of-function mutations in sodium channel Nav1.7 cause anosmia.
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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