| scholarly article | Q13442814 |
| P356 | DOI | 10.1111/J.1399-0004.2007.00790.X |
| P698 | PubMed publication ID | 17470132 |
| P50 | author | Marie-Pierre Dubé | Q30002184 |
| Michael R. Hayden | Q6833706 | ||
| P2093 | author name string | Fraser R | |
| Green R | |||
| Thompson J | |||
| Young C | |||
| Boltshauser E | |||
| Goldberg YP | |||
| Hossain S | |||
| Cox J | |||
| Andria G | |||
| Bowsher D | |||
| Pimstone SN | |||
| Samuels ME | |||
| Younghusband HB | |||
| Donaldson G | |||
| Pape T | |||
| Payne B | |||
| MacFarlane J | |||
| Dimon JH | |||
| Duff A | |||
| Grinspan GA | |||
| Ives E | |||
| Kerdraon J | |||
| MacDonald ML | |||
| Mattice M | |||
| Radomski C | |||
| Sherrington R | |||
| Sibley BG | |||
| Toscano E | |||
| P2860 | cites work | Congenital insensitivity to pain with anhydrosis. A unique syndrome in two male siblings | Q34540401 |
| P433 | issue | 4 | |
| P921 | main subject | congenital disorder | Q727096 |
| P304 | page(s) | 311-319 | |
| P577 | publication date | 2007-04-01 | |
| P1433 | published in | Clinical Genetics | Q5133760 |
| P1476 | title | Loss-of-function mutations in the Nav1.7 gene underlie congenital indifference to pain in multiple human populations | |
| P478 | volume | 71 |
| Q64062398 | A gain-of-function sodium channel β2-subunit mutation in painful diabetic neuropathy |
| Q34263684 | A nonsense mutation in the SCN9A gene in congenital insensitivity to pain |
| Q89441470 | A novel SCN9A splicing mutation in a compound heterozygous girl with congenital insensitivity to pain, hyposmia and hypogeusia |
| Q48215303 | A point mutation at F1737 of the human Nav1.7 sodium channel decreases inhibition by local anesthetics |
| Q39972794 | A pore-blocking hydrophobic motif at the cytoplasmic aperture of the closed-state Nav1.7 channel is disrupted by the erythromelalgia-associated F1449V mutation. |
| Q52425135 | A role for TENM1 mutations in congenital general anosmia. |
| Q33504524 | A role of SCN9A in human epilepsies, as a cause of febrile seizures and as a potential modifier of Dravet syndrome |
| Q40114322 | A stop codon mutation in SCN9A causes lack of pain sensation |
| Q58692119 | Addressing the Issue of Tetrodotoxin Targeting |
| Q27678595 | Analysis of the Structural and Molecular Basis of Voltage-sensitive Sodium Channel Inhibition by the Spider Toxin Huwentoxin-IV ( -TRTX-Hh2a) |
| Q39322438 | Anosmia-A Clinical Review |
| Q33790438 | Association of rare missense variants in the second intracellular loop of NaV1.7 sodium channels with familial autism |
| Q51890503 | Beyond neuropathy in hereditary sensory and autonomic neuropathy type V: cognitive evaluation. |
| Q47785613 | Burn Pain: A Systematic and Critical Review of Epidemiology, Pathophysiology, and Treatment. |
| Q36089877 | Candidate hippocampal biomarkers of susceptibility and resilience to stress in a rat model of depression. |
| Q60066278 | Channelopathies have many faces |
| Q48297578 | Channelopathy: a novel mutation in the SCN9A gene causes insensitivity to pain and autonomic dysregulation |
| Q47113350 | Characterisation of Nav1.7 functional expression in rat dorsal root ganglia neurons by using an electrical field stimulation assay. |
| Q39984138 | Clinical Micro-Dose Studies to Explore the Human Pharmacokinetics of Four Selective Inhibitors of Human Nav1.7 Voltage-Dependent Sodium Channels |
| Q37156284 | Clinical features for diagnosis and management of patients with PRDM12 congenital insensitivity to pain |
| Q54979414 | Co-expression of β Subunits with the Voltage-Gated Sodium Channel NaV1.7: the Importance of Subunit Association and Phosphorylation and Their Effects on Channel Pharmacology and Biophysics. |
| Q36392068 | Cold-aggravated pain in humans caused by a hyperactive NaV1.9 channel mutant |
| Q36727094 | Compound heterozygosity in sodium channel Nav1.7 in a family with hereditary erythermalgia |
| Q35048508 | Comprehensive RNA-Seq expression analysis of sensory ganglia with a focus on ion channels and GPCRs in Trigeminal ganglia |
| Q34443172 | Congenital insensitivity to pain: a case report and review of the literature. |
| Q34254861 | Congenital insensitivity to pain: novel SCN9A missense and in-frame deletion mutations |
| Q36432810 | Conotoxins targeting neuronal voltage-gated sodium channel subtypes: potential analgesics? |
| Q38991080 | Control of Neurotransmission by NaV1.7 in Human, Guinea Pig, and Mouse Airway Parasympathetic Nerves |
| Q37396519 | Current evidence for a modulation of low back pain by human genetic variants |
| Q47219652 | DRG Voltage-gated Sodium Channel 1.7 is Up-regulated in Paclitaxel-Induced Neuropathy in Rats and in Humans with Neuropathic Pain. |
| Q64058142 | Defining the Functional Role of Na1.7 in Human Nociception |
| Q41576564 | Discovery and mode of action of a novel analgesic β-toxin from the African spider Ceratogyrus darlingi |
| Q24605644 | Discovery of a selective NaV1.7 inhibitor from centipede venom with analgesic efficacy exceeding morphine in rodent pain models |
| Q99248373 | Discovery of a selective, state-independent inhibitor of NaV1.7 by modification of guanidinium toxins |
| Q91969140 | Discovery of aryl sulfonamide-selective Nav1.7 inhibitors with a highly hydrophobic ethanoanthracene core |
| Q24650168 | Dynorphin, stress, and depression |
| Q36737802 | Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia |
| Q37065681 | Engineering Highly Potent and Selective Microproteins against Nav1.7 Sodium Channel for Treatment of Pain |
| Q33650951 | Enhanced excitability of primary sensory neurons and altered gene expression of neuronal ion channels in dorsal root ganglion in paclitaxel-induced peripheral neuropathy |
| Q41901986 | Expression of Nav1.7 in DRG neurons extends from peripheral terminals in the skin to central preterminal branches and terminals in the dorsal horn |
| Q41210428 | Extending the clinical spectrum of pain channelopathies |
| Q38162868 | Fruit flies as a powerful model to drive or validate pain genomics efforts. |
| Q90421910 | Functional confirmation that the R1488* variant in SCN9A results in complete loss-of-function of Nav1.7. |
| Q39157361 | Gain-of-function mutation of a voltage-gated sodium channel NaV1.7 associated with peripheral pain and impaired limb development |
| Q38090292 | Genes, molecules and patients--emerging topics to guide clinical pain research |
| Q38026870 | Genetic aspects of sodium channelopathy in small fiber neuropathy |
| Q37120834 | Genetic mutations that prevent pain: implications for future pain medication |
| Q26777559 | Genetic neurological channelopathies: molecular genetics and clinical phenotypes |
| Q37846139 | Genetic variability of pain perception and treatment--clinical pharmacological implications |
| Q37382551 | Genetics and molecular pathophysiology of Na(v)1.7-related pain syndromes |
| Q28542818 | Global Nav1.7 knockout mice recapitulate the phenotype of human congenital indifference to pain |
| Q38030606 | Human Mendelian pain disorders: a key to discovery and validation of novel analgesics. |
| Q104577323 | Human sensory neurons derived from pluripotent stem cells for disease modelling and personalized medicine |
| Q33664676 | Identifying the Ion Channels Responsible for Signaling Gastro-Intestinal Based Pain |
| Q36674682 | Infrequent SCN9A mutations in congenital insensitivity to pain and erythromelalgia. |
| Q48062762 | Inherited erythromelalgia due to mutations in SCN9A: natural history, clinical phenotype and somatosensory profile |
| Q35226085 | Inherited neuronal ion channelopathies: new windows on complex neurological diseases |
| Q28548202 | Inhibition of Inactive States of Tetrodotoxin-Sensitive Sodium Channels Reduces Spontaneous Firing of C-Fiber Nociceptors and Produces Analgesia in Formalin and Complete Freund's Adjuvant Models of Pain |
| Q36287712 | Inhibition of Nav1.7 channels by methyl eugenol as a mechanism underlying its antinociceptive and anesthetic actions |
| Q38265475 | Inhibitors of voltage-gated sodium channel Nav1.7: patent applications since 2010. |
| Q33390819 | Insensitivity to pain induced by a potent selective closed-state Nav1.7 inhibitor |
| Q37855929 | Ion channel blockers for the treatment of neuropathic pain |
| Q37855927 | Isoform-selective voltage-gated Na(+) channel modulators as next-generation analgesics |
| Q37927128 | Isolated and syndromic forms of congenital anosmia |
| Q34850116 | Linkage between increased nociception and olfaction via a SCN9A haplotype |
| Q48496695 | Localization of Nav 1.7 in the normal and injured rodent olfactory system indicates a critical role in olfaction, pheromone sensing and immune function. |
| Q30540365 | Loss-of-function mutations in sodium channel Nav1.7 cause anosmia. |
| Q36281738 | Matrix Metalloproteinase (MMP) Proteolysis of the Extracellular Loop of Voltage-gated Sodium Channels and Potential Alterations in Pain Signaling |
| Q36324512 | Matrix metalloproteinases - From the cleavage data to the prediction tools and beyond |
| Q37368204 | MicroRNA-30b regulates expression of the sodium channel Nav1.7 in nerve injury-induced neuropathic pain in the rat |
| Q88153151 | Modulation of sodium channels as pharmacological tool for pain therapy-highlights and gaps |
| Q36487377 | Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade |
| Q89208606 | Mutation in Nav 1.7 causes high olfactory sensitivity |
| Q38239544 | Mutational consequences of aberrant ion channels in neurological disorders |
| Q59103387 | Mutations in Sodium Channel Gene SCN9A and the Pain Perception Disorders |
| Q34585790 | Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders |
| Q46301976 | NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders. |
| Q41978464 | NaV1.7: stress-induced changes in immunoreactivity within magnocellular neurosecretory neurons of the supraoptic nucleus |
| Q37287580 | Nature and nurture of human pain |
| Q33329730 | Nav1.7 expression is increased in painful human dental pulp |
| Q35003780 | Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons |
| Q36091952 | Navβ4 regulates fast resurgent sodium currents and excitability in sensory neurons |
| Q38033634 | Nerve growth factor and the physiology of pain: lessons from congenital insensitivity to pain with anhidrosis |
| Q38042001 | Neurological perspectives on voltage-gated sodium channels. |
| Q42065325 | Novel mRNA isoforms of the sodium channels Na(v)1.2, Na(v)1.3 and Na(v)1.7 encode predicted two-domain, truncated proteins |
| Q42078485 | Null mutation in SCN9A in which noxious stimuli can be detected in the absence of pain. |
| Q39278452 | Overcoming obstacles to developing new analgesics |
| Q24622323 | Pain as a channelopathy |
| Q37943756 | Pain disorders and erythromelalgia caused by voltage-gated sodium channel mutations |
| Q33739909 | Pain perception is altered by a nucleotide polymorphism in SCN9A |
| Q53504369 | Pain thresholds, supra-threshold pain and lidocaine sensitivity in patients with erythromelalgia, including the I848Tmutation in NaV 1.7. |
| Q38552593 | Pain without nociceptors? Nav1.7-independent pain mechanisms. |
| Q37944353 | Pain, analgesia and genetics. |
| Q38210568 | Painful and painless channelopathies. |
| Q38253772 | Painful neuropathies: the emerging role of sodium channelopathies |
| Q36916035 | Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable |
| Q34316700 | Pharmacogenomic considerations in opioid analgesia. |
| Q30835612 | Pharmacological characterisation of the highly NaV1.7 selective spider venom peptide Pn3a |
| Q55037976 | Pharmacological characterization of potent and selective NaV1.7 inhibitors engineered from Chilobrachys jingzhao tarantula venom peptide JzTx-V. |
| Q26784432 | Primary erythromelalgia: a review |
| Q24289028 | Progress in genetic studies of pain and analgesia |
| Q34612092 | Ranolazine attenuates behavioral signs of neuropathic pain |
| Q90258766 | Rat NaV1.7 loss-of-function genetic model: Deficient nociceptive and neuropathic pain behavior with retained olfactory function and intra-epidermal nerve fibers |
| Q41998701 | Safety and Efficacy of a Topical Sodium Channel Inhibitor (TV-45070) in Patients With Postherpetic Neuralgia (PHN): A Randomized, Controlled, Proof-of-Concept, Crossover Study, With a Subgroup Analysis of the Nav1.7 R1150W Genotype |
| Q38207566 | Saxitoxin. |
| Q38088356 | Screening TRPV1 antagonists for the treatment of pain: lessons learned over a decade |
| Q37855923 | Screening technologies for ion channel drug discovery |
| Q37424935 | Shellfish toxins targeting voltage-gated sodium channels |
| Q35554540 | Short-lasting unilateral neuralgiform headache attacks with ispilateral facial flushing is a new variant of paroxysmal extreme pain disorder |
| Q41661778 | Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability |
| Q37318012 | Sodium channel Nav1.7 expression is upregulated in the dorsal root ganglia in a rat model of paclitaxel-induced peripheral neuropathy |
| Q37605350 | Sodium channel blockers for the treatment of neuropathic pain |
| Q38260278 | Sodium channel genes in pain-related disorders: phenotype-genotype associations and recommendations for clinical use. |
| Q37681340 | Sodium channelopathies and pain |
| Q37992862 | Sodium channels, the electrogenisome and the electrogenistat: lessons and questions from the clinic |
| Q35155666 | Spider-venom peptides as therapeutics. |
| Q101038915 | Status of peripheral sodium channel blockers for non-addictive pain treatment |
| Q83227877 | Stereotyped transcriptomic transformation of somatosensory neurons in response to injury |
| Q37618893 | Subtype-selective targeting of voltage-gated sodium channels |
| Q39150711 | Synergistic combinations of the dual enkephalinase inhibitor PL265 given orally with various analgesic compounds acting on different targets, in a murine model of cancer-induced bone pain |
| Q38165856 | Targeting voltage gated sodium channels NaV1.7, Na V1.8, and Na V1.9 for treatment of pathological cough |
| Q36258703 | The AMPK Activator A769662 Blocks Voltage-Gated Sodium Channels: Discovery of a Novel Pharmacophore with Potential Utility for Analgesic Development |
| Q38066723 | The Na(V)1.7 sodium channel: from molecule to man. |
| Q64108951 | The Role of Toxins in the Pursuit for Novel Analgesics |
| Q27011310 | The perception and endogenous modulation of pain |
| Q42611687 | The phenotype of congenital insensitivity to pain due to the NaV1.9 variant p.L811P. |
| Q34674268 | The roles of sodium channels in nociception: Implications for mechanisms of pain |
| Q37379467 | Thermosensory and mechanosensory perception in human genetic disease |
| Q38239812 | Translational pain research: Lessons from genetics and genomics |
| Q34300278 | Two novel mutations of SCN9A (Nav1.7) are associated with partial congenital insensitivity to pain |
| Q33586810 | Upregulation of nav1.7 through high salt loading: (mol pain 2013;9:39) |
| Q39010857 | Visceral and somatic pain modalities reveal NaV 1.7-independent visceral nociceptive pathways |
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| Q48273674 | Voltage-gated sodium channels: (NaV )igating the field to determine their contribution to visceral nociception. |
| Q53404165 | [Sensory and autonomic neuropathies and pain-related channelopathies]. |
| Q45384168 | µ-Conotoxins Modulating Sodium Currents in Pain Perception and Transmission: A Therapeutic Potential |
| Q58085867 | µ-TRTX-Ca1a: a novel neurotoxin from Cyriopagopus albostriatus with analgesic effects |
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