Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable - Wikidata - wikimedia - TriplyDB

Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable

Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable

http://www.wikidata.org/entity/Q36916035

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Primary erythromelalgia: a review Comparison of Gating Properties and Use-Dependent Block of Nav1.5 and Nav1.7 Channels by Anti-Arrhythmics Mexiletine and Lidocaine Relationship of axonal voltage-gated sodium channel 1.8 (NaV1.8) mRNA accumulation to sciatic nerve injury-induced painful neuropathy in rats Structure-based assessment of disease-related mutations in human voltage-gated sodium channels.Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T.Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders Synthesis and analgesic effects of μ-TRTX-Hhn1b on models of inflammatory and neuropathic pain.Ion channelopathies in functional GI disorders.Inhibition of Navβ4 peptide-mediated resurgent sodium currents in Nav1.7 channels by carbamazepine, riluzole, and anandamide.Novel SCN9A mutations underlying extreme pain phenotypes: unexpected electrophysiological and clinical phenotype correlations.Sodium channel Nav1.7 in vascular myocytes, endothelium, and innervating axons in human skin.Navβ4 regulates fast resurgent sodium currents and excitability in sensory neurons Pharmacogenetics of analgesic drugs The AMPK Activator A769662 Blocks Voltage-Gated Sodium Channels: Discovery of a Novel Pharmacophore with Potential Utility for Analgesic Development.Network topology of NaV1.7 mutations in sodium channel-related painful disorders.Novel mutations mapping to the fourth sodium channel domain of Nav1.7 result in variable clinical manifestations of primary erythromelalgia MicroRNA-30b regulates expression of the sodium channel Nav1.7 in nerve injury-induced neuropathic pain in the rat Thermosensory and mechanosensory perception in human genetic disease.Pain disorders and erythromelalgia caused by voltage-gated sodium channel mutations.Recent developments regarding voltage-gated sodium channel blockers for the treatment of inherited and acquired neuropathic pain syndromes.Neurological perspectives on voltage-gated sodium channels.Mutational consequences of aberrant ion channels in neurological disorders.Translational pain research: Lessons from genetics and genomics.What are the treatment options for paroxysmal extreme pain disorder?Analgesic Effects of GpTx-1, PF-04856264 and CNV1014802 in a Mouse Model of NaV1.7-Mediated Pain.Effects of ranolazine on wild-type and mutant hNav1.7 channels and on DRG neuron excitability.Molecular architecture of a sodium channel S6 helix: radial tuning of the voltage-gated sodium channel 1.7 activation gate Extending the clinical spectrum of pain channelopathies.Contrasting effects of phosphatidylinositol 4,5-bisphosphate on cloned TMEM16A and TMEM16B channels.Discovery and mode of action of a novel analgesic β-toxin from the African spider Ceratogyrus darlingi.Expression of Nav1.7 in DRG neurons extends from peripheral terminals in the skin to central preterminal branches and terminals in the dorsal horn.NaV1.7: stress-induced changes in immunoreactivity within magnocellular neurosecretory neurons of the supraoptic nucleus.Paroxysmal extreme pain disorder: a molecular lesion of peripheral neurons.Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Nav1.7 mutation that massively hyperpolarizes activation.Nonlinear effects of hyperpolarizing shifts in activation of mutant Nav1.7 channels on resting membrane potential.Early- and late-onset inherited erythromelalgia: genotype-phenotype correlation.Channelopathy: a novel mutation in the SCN9A gene causes insensitivity to pain and autonomic dysregulation.Small nerve fibres, small hands and small feet: a new syndrome of pain, dysautonomia and acromesomelia in a kindred with a novel NaV1.7 mutation.Flushing Disorders Associated with Gastrointestinal Symptoms: Part 2, Systemic Miscellaneous Conditions.Enhancing inactivation rather than reducing activation of Nav1.7 channels by a clinically effective analgesic CNV1014802.

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P2860

Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable

http://www.wikidata.org/entity/Q36916035

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Paroxysmal extreme pain disord ...... ers DRG neurons hyperexcitable

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Brian W Jarecki

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Lynda Tyrrell

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Mark Lawden

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Stephen G Waxman

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Sulayman D Dib-Hajj

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Tanya Z Fischer

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Theodore R Cummins

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P2860

Structure and functional expression of a new member of the tetrodotoxin-sensitive voltage-activated sodium channel family from human neuroendocrine cells

Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain

Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia

A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity

SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes

Spectrum of SCN1A mutations in severe myoclonic epilepsy of infancy

Paroxysmal extreme pain disorder (previously familial rectal pain syndrome)

From genes to pain: Na v 1.7 and human pain disorders

An SCN9A channelopathy causes congenital inability to experience pain

Identification of PN1, a predominant voltage-dependent sodium channel expressed principally in peripheral neurons

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