226 related articles for article (PubMed ID: 23383113)
1. A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockers.
Wu MT; Huang PY; Yen CT; Chen CC; Lee MJ
PLoS One; 2013; 8(1):e55212. PubMed ID: 23383113
[TBL] [Abstract][Full Text] [Related]
2. Nav1.7-A1632G Mutation from a Family with Inherited Erythromelalgia: Enhanced Firing of Dorsal Root Ganglia Neurons Evoked by Thermal Stimuli.
Yang Y; Huang J; Mis MA; Estacion M; Macala L; Shah P; Schulman BR; Horton DB; Dib-Hajj SD; Waxman SG
J Neurosci; 2016 Jul; 36(28):7511-22. PubMed ID: 27413160
[TBL] [Abstract][Full Text] [Related]
3. A Novel SCN9A Mutation (F826Y) in Primary Erythromelalgia Alters the Excitability of Nav1.7.
Wu B; Zhang Y; Tang H; Yang M; Long H; Shi G; Tang J; Shi X
Curr Mol Med; 2017; 17(6):450-457. PubMed ID: 28990532
[TBL] [Abstract][Full Text] [Related]
4. Anomalous enhancement of resurgent Na
Huang CW; Lai HJ; Huang PY; Lee MJ; Kuo CC
Sci Rep; 2019 Aug; 9(1):12251. PubMed ID: 31439884
[TBL] [Abstract][Full Text] [Related]
5. Novel mutations mapping to the fourth sodium channel domain of Nav1.7 result in variable clinical manifestations of primary erythromelalgia.
Cregg R; Laguda B; Werdehausen R; Cox JJ; Linley JE; Ramirez JD; Bodi I; Markiewicz M; Howell KJ; Chen YC; Agnew K; Houlden H; Lunn MP; Bennett DL; Wood JN; Kinali M
Neuromolecular Med; 2013 Jun; 15(2):265-78. PubMed ID: 23292638
[TBL] [Abstract][Full Text] [Related]
6. Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade.
Cheng X; Dib-Hajj SD; Tyrrell L; Waxman SG
Mol Pain; 2008 Jan; 4():1. PubMed ID: 18171466
[TBL] [Abstract][Full Text] [Related]
7. Mexiletine as a treatment for primary erythromelalgia: normalization of biophysical properties of mutant L858F NaV 1.7 sodium channels.
Cregg R; Cox JJ; Bennett DL; Wood JN; Werdehausen R
Br J Pharmacol; 2014 Oct; 171(19):4455-63. PubMed ID: 24866741
[TBL] [Abstract][Full Text] [Related]
8. A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity.
Sheets PL; Jackson JO; Waxman SG; Dib-Hajj SD; Cummins TR
J Physiol; 2007 Jun; 581(Pt 3):1019-31. PubMed ID: 17430993
[TBL] [Abstract][Full Text] [Related]
9. A new Nav1.7 mutation in an erythromelalgia patient.
Estacion M; Yang Y; Dib-Hajj SD; Tyrrell L; Lin Z; Yang Y; Waxman SG
Biochem Biophys Res Commun; 2013 Mar; 432(1):99-104. PubMed ID: 23376079
[TBL] [Abstract][Full Text] [Related]
10. Inherited pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation.
Eberhardt M; Nakajima J; Klinger AB; Neacsu C; Hühne K; O'Reilly AO; Kist AM; Lampe AK; Fischer K; Gibson J; Nau C; Winterpacht A; Lampert A
J Biol Chem; 2014 Jan; 289(4):1971-80. PubMed ID: 24311784
[TBL] [Abstract][Full Text] [Related]
11. Novel SCN9A mutations underlying extreme pain phenotypes: unexpected electrophysiological and clinical phenotype correlations.
Emery EC; Habib AM; Cox JJ; Nicholas AK; Gribble FM; Woods CG; Reimann F
J Neurosci; 2015 May; 35(20):7674-81. PubMed ID: 25995458
[TBL] [Abstract][Full Text] [Related]
12. Dynamic-clamp analysis of wild-type human Nav1.7 and erythromelalgia mutant channel L858H.
Vasylyev DV; Han C; Zhao P; Dib-Hajj S; Waxman SG
J Neurophysiol; 2014 Apr; 111(7):1429-43. PubMed ID: 24401712
[TBL] [Abstract][Full Text] [Related]
13. Structural basis for severe pain caused by mutations in the S4-S5 linkers of voltage-gated sodium channel Na
Wisedchaisri G; Gamal El-Din TM; Zheng N; Catterall WA
Proc Natl Acad Sci U S A; 2023 Apr; 120(14):e2219624120. PubMed ID: 36996107
[TBL] [Abstract][Full Text] [Related]
14. Mexiletine-responsive erythromelalgia due to a new Na(v)1.7 mutation showing use-dependent current fall-off.
Choi JS; Zhang L; Dib-Hajj SD; Han C; Tyrrell L; Lin Z; Wang X; Yang Y; Waxman SG
Exp Neurol; 2009 Apr; 216(2):383-9. PubMed ID: 19162012
[TBL] [Abstract][Full Text] [Related]
15. Erythromelalgia caused by the missense mutation p.Arg220Pro in an alternatively spliced exon of SCN9A (NaV1.7).
Deuis JR; Kumble S; Keramidas A; Ragnarsson L; Simons C; Pais L; White SM; Vetter I
Hum Mol Genet; 2024 Jan; 33(2):103-109. PubMed ID: 37721535
[TBL] [Abstract][Full Text] [Related]
16. Specific changes in conduction velocity recovery cycles of single nociceptors in a patient with erythromelalgia with the I848T gain-of-function mutation of Nav1.7.
Namer B; Ørstavik K; Schmidt R; Kleggetveit IP; Weidner C; Mørk C; Kvernebo MS; Kvernebo K; Salter H; Carr TH; Segerdahl M; Quiding H; Waxman SG; Handwerker HO; Torebjörk HE; Jørum E; Schmelz M
Pain; 2015 Sep; 156(9):1637-1646. PubMed ID: 25993546
[TBL] [Abstract][Full Text] [Related]
17. Gain-of-function mutation of a voltage-gated sodium channel Na
Tanaka BS; Nguyen PT; Zhou EY; Yang Y; Yarov-Yarovoy V; Dib-Hajj SD; Waxman SG
J Biol Chem; 2017 Jun; 292(22):9262-9272. PubMed ID: 28381558
[TBL] [Abstract][Full Text] [Related]
18. Temperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7.
Han C; Lampert A; Rush AM; Dib-Hajj SD; Wang X; Yang Y; Waxman SG
Mol Pain; 2007 Jan; 3():3. PubMed ID: 17239250
[TBL] [Abstract][Full Text] [Related]
19. Primary erythromelalgia in a 12-year-old boy: positive response to sodium channel blockers despite negative SCN9A mutations.
Jakob A; Creutzfeldt R; Staszewski O; Winterpacht A; Berner R; Hufnagel M
Klin Padiatr; 2012 Sep; 224(5):309-12. PubMed ID: 22170168
[TBL] [Abstract][Full Text] [Related]
20. Genetic, electrophysiological, and pathological studies on patients with SCN9A-related pain disorders.
Yuan JH; Cheng X; Matsuura E; Higuchi Y; Ando M; Hashiguchi A; Yoshimura A; Nakachi R; Mine J; Taketani T; Maeda K; Kawakami S; Kira R; Tanaka S; Kanai K; Dib-Hajj F; Dib-Hajj SD; Waxman SG; Takashima H
J Peripher Nerv Syst; 2023 Dec; 28(4):597-607. PubMed ID: 37555797
[TBL] [Abstract][Full Text] [Related]
[Next] [New Search]
