Gain-of-function Nav1.8 mutations in painful neuropathy. - Wikidata - awgldk - TriplyDB

Gain-of-function Nav1.8 mutations in painful neuropathy.

Gain-of-function Nav1.8 mutations in painful neuropathy.

http://www.wikidata.org/entity/Q34309236

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Therapeutic Approaches to Genetic Ion Channelopathies and Perspectives in Drug Discovery Conotoxins That Could Provide Analgesia through Voltage Gated Sodium Channel Inhibition Genetic neurological channelopathies: molecular genetics and clinical phenotypes.Neuropathic Pain due to Small Fiber Neuropathy in Aging: Current Management and Future Prospects Molecular pathophysiology and pharmacology of the voltage-sensing module of neuronal ion channels The clinical approach to small fibre neuropathy and painful channelopathy Nav1.7 and other voltage-gated sodium channels as drug targets for pain relief A de novo gain-of-function mutation in SCN11A causes loss of pain perception Global Nav1.7 knockout mice recapitulate the phenotype of human congenital indifference to pain Infantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese Families Selective spider toxins reveal a role for the Nav1.1 channel in mechanical pain A gain-of-function voltage-gated sodium channel 1.8 mutation drives intense hyperexcitability of A- and C-fiber neurons.Structure-based assessment of disease-related mutations in human voltage-gated sodium channels.Dysregulation of voltage-gated sodium channels by ubiquitin ligase NEDD4-2 in neuropathic pain.Exon 11 skipping of SCN10A coding for voltage-gated sodium channels in dorsal root ganglia Pain related channels are differentially expressed in neuronal and non-neuronal cells of glabrous skin of fabry knockout male mice Lost but making progress--Where will new analgesic drugs come from?Herbal medicines for the treatment of cancer chemotherapy-induced side effects.A novel selective and orally bioavailable Nav 1.8 channel blocker, PF-01247324, attenuates nociception and sensory neuron excitability.Human Na(v)1.8: enhanced persistent and ramp currents contribute to distinct firing properties of human DRG neurons.No Fabry Disease in Patients Presenting with Isolated Small Fiber Neuropathy Human pain and genetics: some basics SCN10A Mutation in a Patient with Erythromelalgia Enhances C-Fiber Activity Dependent Slowing.Post-translational modifications of voltage-gated sodium channels in chronic pain syndromes Cold-aggravated pain in humans caused by a hyperactive NaV1.9 channel mutant.Congenital insensitivity to pain: Fracturing without apparent skeletal pathobiology caused by an autosomal dominant, second mutation in SCN11A encoding voltage-gated sodium channel 1.9.Designing a C84 fullerene as a specific voltage-gated sodium channel blocker Efficacy, safety, and tolerability of lacosamide in patients with gain-of-function Nav1.7 mutation-related small fiber neuropathy: study protocol of a randomized controlled trial-the LENSS study.EXPRESS: Voltage-dependent sodium (NaV) channels in group IV sensory afferents.The CRISPR/Cas9 system for gene editing and its potential application in pain research Advanced Genetic Testing Comes to the Pain Clinic to Make a Diagnosis of Paroxysmal Extreme Pain Disorder.A SCN10A SNP biases human pain sensitivity.Gain-of-function mutations in SCN11A cause familial episodic pain.Sodium channel Nav1.7 expression is upregulated in the dorsal root ganglia in a rat model of paclitaxel-induced peripheral neuropathy.Pathological nociceptors in two patients with erythromelalgia-like symptoms and rare genetic Nav 1.9 variants A painful neuropathy-associated Nav1.7 mutant leads to time-dependent degeneration of small-diameter axons associated with intracellular Ca2+ dysregulation and decrease in ATP levels.Antinociceptive Effects of AGAP, a Recombinant Neurotoxic Polypeptide: Possible Involvement of the Tetrodotoxin-Resistant Sodium Channels in Small Dorsal Root Ganglia Neurons.Biallelic SCN10A mutations in neuromuscular disease and epileptic encephalopathy.Recent genetic discoveries implicating ion channels in human cardiovascular diseases Painful and painless diabetic neuropathy: one disease or two?

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Gain-of-function Nav1.8 mutations in painful neuropathy.

http://www.wikidata.org/entity/Q34309236

description

2012 nî lūn-bûn

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2012 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2012 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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name

Gain-of-function Nav1.8 mutations in painful neuropathy.

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Gain-of-function Nav1.8 mutations in painful neuropathy.

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Gain-of-function Nav1.8 mutations in painful neuropathy.

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type

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Gain-of-function Nav1.8 mutations in painful neuropathy.

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Gain-of-function Nav1.8 mutations in painful neuropathy.

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Gain-of-function Nav1.8 mutations in painful neuropathy.

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prefLabel

Gain-of-function Nav1.8 mutations in painful neuropathy.

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Gain-of-function Nav1.8 mutations in painful neuropathy.

@en

Gain-of-function Nav1.8 mutations in painful neuropathy.

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PNAS.1216080109

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Proceedings of the National Academy of Sciences of the United States of America

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Gain-of-function Nav1.8 mutations in painful neuropathy

@en

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Anna-Karin Persson

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Chongyang Han

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Dimos Kapetis

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Hye-Sook Ahn

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Ingemar S J Merkies

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Janneke G J Hoeijmakers

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Monique M Gerrits

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Raffaella Lombardi

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Stephen G Waxman

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Sulayman D Dib-Hajj

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P2860

Neuronal sodium-channel alpha1-subunit mutations in generalized epilepsy with febrile seizures plus.

A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons

Mutations of neuronal voltage-gated Na+ channel alpha 1 subunit gene SCN1A in core severe myoclonic epilepsy in infancy (SMEI) and in borderline SMEI (SMEB)

Neurobiology: a channel sets the gain on pain

Intraepidermal nerve fiber density at the distal leg: a worldwide normative reference study

A tetrodotoxin-resistant voltage-gated sodium channel expressed by sensory neurons

Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy

Low density of sodium channels supports action potential conduction in axons of neonatal rat optic nerve.

The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways.

A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia.

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10.1073/PNAS.1216080109

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47

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109

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Giuseppe Lauria

Catharina G Faber

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2012-10-31T00:00:00Z

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232745987

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23115331

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