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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 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, ACID, HAD, V1a, Plasminogen
Papers on PN1
Isolation, synthesis and characterization of ω-TRTX-Cc1a, a novel tarantula venom peptide that selectively targets L-type Cav channels.
Rash et al., Australia. In Biochem Pharmacol, Jun 2014
Cc1a exhibited weak activity at NaV1.5 and NaV1.7 voltage-gated sodium (NaV) channels stably expressed in mammalian HEK or CHO cells, respectively.
Regulation and pharmacological blockade of sodium-potassium ATPase: a novel pathway to neuropathy.
Gould et al., New Orleans, United States. In J Neurol Sci, Jun 2014
Inflammation causes upregulation of NaV1.7 sodium channels in the associated dorsal root ganglia (DRG).
Furanocoumarins are a novel class of modulators for the transient receptor potential vanilloid type 1 (TRPV1) channel.
Obukhov et al., In J Biol Chem, May 2014
Conversely, imperatorin sensitized TRPV1 to acid activation but did not affect the current amplitude and/or the activation-inactivation properties of Na(v)1.7, a channel important for transmission of nociceptive information.
The endocannabinoid anandamide inhibits voltage-gated sodium channels Nav1.2, Nav1.6, Nav1.7, and Nav1.8 in Xenopus oocytes.
Sata et al., Tokyo, Japan. In Anesth Analg, Mar 2014
Nav1.6, Nav1.7, and Nav1.8, to explore the mechanisms underlying the antinociceptive effects of anandamide.
Purification and refolding of anti-T-antigen single chain antibodies (scFvs) expressed in Escherichia coli as inclusion bodies.
Fujita-Yamaguchi et al., Funaishikawa, Japan. In Biosci Trends, Feb 2014
Inclusion bodies isolated from E. coli cells were denatured in 3.5 M Gdn-HCl.
An atypical case of SCN9A mutation presenting with global motor delay and a severe pain disorder.
Rossignol et al., Montréal, Canada. In Muscle Nerve, Jan 2014
INTRODUCTION: Erythromelalgia due to heterozygous gain-of-function SCN9A mutations usually presents as a pure sensory-autonomic disorder characterized by recurrent episodes of burning pain and redness of the extremities.
Genetic determinants of chronic obstructive pulmonary disease in South Indian male smokers.
Kanala et al., Tirupati, India. In Plos One, Dec 2013
Genotype analysis showed association of rs2276109 (MMP12) under additive and dominant models (p = 0.017, p = 0.012 respectively), rs1800925 (IL13) under additive model (p = 0.047) and under recessive model, rs1695 (GSTP1; p = 0.034), rs729631, rs975278, rs7583463 (SERPINE2; p = 0.024, 0.024 and 0.012 respectively), rs2568494, rs10851906 (IREB2; p = 0.026 and 0.041 respectively) and rs7671167 (FAM13A; p = 0.029).
Voltage-gated sodium channel in grasshopper mice defends against bark scorpion toxin.
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.
Painful Na-channelopathies: an expanding universe.
Waxman, New Haven, United States. In Trends Mol Med, Jul 2013
We have learned that mutations of NaV1.8, as well as mutations of NaV1.7, can cause painful Na-channelopathies.
Thrombin inhibition by the serpins.
Huntington, Cambridge, United Kingdom. In J Thromb Haemost, Jun 2013
Although antithrombin (AT), protein C inhibitor (PCI), heparin cofactor II (HCII) and protease nexin-1 (PN1) all share a common fold and mechanism of protease inhibition, they have evolved radically different mechanisms for cofactor-assisted thrombin recognition.
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
Small fibre neuropathy.
Faber et al., Milano, Italy. In Curr Opin Neurol, 2012
An exciting advance has been the identification of gain-of-function mutations in the SCN9A gene encoding for Nav1.7 sodium channel in patients with SFN, leading to the definition of a new genetic channelopathy.
Human Mendelian pain disorders: a key to discovery and validation of novel analgesics.
Hayden et al., Canada. In Clin Genet, 2012
By studying a very rare Mendelian disorder of absent pain perception, congenital indifference to pain, we have defined Nav1.7 (endocded by SCN9A) as a critical and novel target for analgesic development.
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.
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
An SCN9A channelopathy causes congenital inability to experience pain.
Woods et al., Cambridge, United Kingdom. In Nature, 2007
data suggest that SCN9A is an essential and non-redundant requirement for nociception in humans
Induction of glia-derived nexin after lesion of a peripheral nerve.
Monard et al., Basel, Switzerland. In Nature, 1989
Glia-derived nexin (GDN), also known as protease nexin I, is a serine protease inhibitor of deduced relative molecular mass 41,700, identified in conditioned media of glioma cells by its neurite-promoting activity.
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