SCN9A mutations define primary erythermalgia as a neuropathic disorder of voltage gated sodium channels.
about
Temperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7A single sodium channel mutation produces hyper- or hypoexcitability in different types of neuronsA Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivityPain perception is altered by a nucleotide polymorphism in SCN9AAssociation of rare missense variants in the second intracellular loop of NaV1.7 sodium channels with familial autism.Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T.Challenges in the development of novel treatment strategies for neuropathic pain.A nonsense mutation in the SCN9A gene in congenital insensitivity to painSize matters: Erythromelalgia mutation S241T in Nav1.7 alters channel gating.A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockersMutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders.The roles of sodium channels in nociception: Implications for mechanisms of painMassage therapy techniques as pain management for erythromelalgia: a case reportIntra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7.Navβ4 regulates fast resurgent sodium currents and excitability in sensory neuronsImaging the neural correlates of neuropathic pain and pleasurable relief associated with inherited erythromelalgia in a single subject with quantitative arterial spin labelling.Network topology of NaV1.7 mutations in sodium channel-related painful disorders.Infrequent SCN9A mutations in congenital insensitivity to pain and erythromelalgia.Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons.Compound heterozygosity in sodium channel Nav1.7 in a family with hereditary erythermalgiaParoxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitableAdvanced Genetic Testing Comes to the Pain Clinic to Make a Diagnosis of Paroxysmal Extreme Pain Disorder.Nature and nurture of human pain.Inherited pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation.Pain disorders and erythromelalgia caused by voltage-gated sodium channel mutations.Advances in targeting voltage-gated sodium channels with small molecules.Mutational consequences of aberrant ion channels in neurological disorders.The role of sodium channels in painful diabetic and idiopathic neuropathy.Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation.A stop codon mutation in SCN9A causes lack of pain sensation.Extending the clinical spectrum of pain channelopathies.Sodium channel slow inactivation interferes with open channel block.Expression of Nav1.7 in DRG neurons extends from peripheral terminals in the skin to central preterminal branches and terminals in the dorsal horn.Hansen's disease associated with erythromelalgia mimicking Lupus erythematosus.Erythromelalgia mutation Q875E Stabilizes the activated state of sodium channel Nav1.7.Autonomic dysfunction in SCN9A-associated primary erythromelalgia.Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy.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.Genetic studies of human neuropathic pain conditions: a review.
P2860
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P2860
SCN9A mutations define primary erythermalgia as a neuropathic disorder of voltage gated sodium channels.
description
2005 nî lūn-bûn
@nan
2005 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
SCN9A mutations define primary ...... voltage gated sodium channels.
@ast
SCN9A mutations define primary ...... voltage gated sodium channels.
@en
SCN9A mutations define primary ...... voltage gated sodium channels.
@nl
type
label
SCN9A mutations define primary ...... voltage gated sodium channels.
@ast
SCN9A mutations define primary ...... voltage gated sodium channels.
@en
SCN9A mutations define primary ...... voltage gated sodium channels.
@nl
prefLabel
SCN9A mutations define primary ...... voltage gated sodium channels.
@ast
SCN9A mutations define primary ...... voltage gated sodium channels.
@en
SCN9A mutations define primary ...... voltage gated sodium channels.
@nl
P2093
P1476
SCN9A mutations define primary ...... voltage gated sodium channels.
@en
P2093
Alain Taieb
Gerard Guillet
Jan B M J Jansen
Joost P H Drenth
R Lee Kirby
Rene H M te Morsche
P304
P356
10.1111/J.0022-202X.2005.23737.X
P407
P577
2005-06-01T00:00:00Z
P6179
1037998058