Gain-of-function mutations in SCN11A cause familial episodic pain.
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Alternative RNA splicing: contribution to pain and potential therapeutic strategyTherapeutic Approaches to Genetic Ion Channelopathies and Perspectives in Drug DiscoveryConotoxins That Could Provide Analgesia through Voltage Gated Sodium Channel InhibitionGenetic neurological channelopathies: molecular genetics and clinical phenotypes.Molecular pathophysiology and pharmacology of the voltage-sensing module of neuronal ion channelsNav1.7 and other voltage-gated sodium channels as drug targets for pain reliefInfantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese FamiliesSelective spider toxins reveal a role for the Nav1.1 channel in mechanical painStructure-based assessment of disease-related mutations in human voltage-gated sodium channels.Multiple roles for NaV1.9 in the activation of visceral afferents by noxious inflammatory, mechanical, and human disease-derived stimuli.Whole exome sequencing in females with autism implicates novel and candidate genes.Novel sodium channel antagonists in the treatment of neuropathic pain.Post-translational modifications of voltage-gated sodium channels in chronic pain syndromesCold-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.P2Y Receptors Sensitize Mouse and Human Colonic Nociceptors.The CRISPR/Cas9 system for gene editing and its potential application in pain researchPathological nociceptors in two patients with erythromelalgia-like symptoms and rare genetic Nav 1.9 variantsBiophysics, pathophysiology, and pharmacology of ion channel gating pores.Translational pain research: Lessons from genetics and genomics.Painful neuropathies: the emerging role of sodium channelopathies.Progress in the treatment of small fiber peripheral neuropathy.Therapeutic conotoxins: a US patent literature survey.The voltage-gated sodium channel NaV 1.9 in visceral pain.Voltage gated sodium channels as drug discovery targetsHeterologous expression of NaV1.9 chimeras in various cell systems.Gain-of-function mutation p.Arg225Cys in SCN11A causes familial episodic pain and contributes to essential tremor.The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy.Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability.Correlation of the electrophysiological profiles and sodium channel transcripts of individual rat dorsal root ganglia neurons.SCN11A variants may influence postoperative pain sensitivity after gynecological surgery in Chinese Han female patients.The phenotype of congenital insensitivity to pain due to the NaV1.9 variant p.L811P.Gain-of-function mutations in sodium channel Na(v)1.9 in painful neuropathy.The role of Nav1.9 channel in the development of neuropathic orofacial pain associated with trigeminal neuralgia.Electrophysiological and Pharmacological Analyses of Nav1.9 Voltage-Gated Sodium Channel by Establishing a Heterologous Expression System.NaV channel variants in patients with painful and nonpainful peripheral neuropathy.Age-dependent expression of Nav1.9 channels in medial prefrontal cortex pyramidal neurons in rats.Sodium channels in pain disorders: pathophysiology and prospects for treatment.Voltage-gated sodium channels: (NaV )igating the field to determine their contribution to visceral nociception.Pain-Causing Venom Peptides: Insights into Sensory Neuron Pharmacology.
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Gain-of-function mutations in SCN11A cause familial episodic pain.
description
article científic
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article scientifique
@fr
articolo scientifico
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artigo científico
@pt
bilimsel makale
@tr
scientific article published on 24 October 2013
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vedecký článok
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vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
Gain-of-function mutations in SCN11A cause familial episodic pain.
@en
Gain-of-function mutations in SCN11A cause familial episodic pain.
@nl
type
label
Gain-of-function mutations in SCN11A cause familial episodic pain.
@en
Gain-of-function mutations in SCN11A cause familial episodic pain.
@nl
prefLabel
Gain-of-function mutations in SCN11A cause familial episodic pain.
@en
Gain-of-function mutations in SCN11A cause familial episodic pain.
@nl
P2093
P2860
P1476
Gain-of-function mutations in SCN11A cause familial episodic pain.
@en
P2093
Cheng Wang
Hongying Ma
Jing Yu Liu
Jingmin Wen
Kaikai Ran
Liang Hong Zheng
P2860
P304
P356
10.1016/J.AJHG.2013.09.016
P407
P577
2013-10-24T00:00:00Z