234 related articles for article (PubMed ID: 32663327)
1. Uncoupling sodium channel dimers restores the phenotype of a pain-linked Na
Rühlmann AH; Körner J; Hausmann R; Bebrivenski N; Neuhof C; Detro-Dassen S; Hautvast P; Benasolo CA; Meents J; Machtens JP; Schmalzing G; Lampert A
Br J Pharmacol; 2020 Oct; 177(19):4481-4496. PubMed ID: 32663327
[TBL] [Abstract][Full Text] [Related]
2. 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]
3. NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders.
Estacion M; Dib-Hajj SD; Benke PJ; Te Morsche RH; Eastman EM; Macala LJ; Drenth JP; Waxman SG
J Neurosci; 2008 Oct; 28(43):11079-88. PubMed ID: 18945915
[TBL] [Abstract][Full Text] [Related]
4. 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]
5. 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]
6. 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]
7. Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents.
Kriegeskorte S; Bott R; Hampl M; Korngreen A; Hausmann R; Lampert A
J Gen Physiol; 2023 Sep; 155(9):. PubMed ID: 37531097
[TBL] [Abstract][Full Text] [Related]
8. Sodium channel slow inactivation interferes with open channel block.
Hampl M; Eberhardt E; O'Reilly AO; Lampert A
Sci Rep; 2016 May; 6():25974. PubMed ID: 27174182
[TBL] [Abstract][Full Text] [Related]
9. 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]
10. 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]
11. Inhibition of Navβ4 peptide-mediated resurgent sodium currents in Nav1.7 channels by carbamazepine, riluzole, and anandamide.
Theile JW; Cummins TR
Mol Pharmacol; 2011 Oct; 80(4):724-34. PubMed ID: 21788423
[TBL] [Abstract][Full Text] [Related]
12. Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation.
Jarecki BW; Sheets PL; Jackson JO; Cummins TR
J Physiol; 2008 Sep; 586(17):4137-53. PubMed ID: 18599537
[TBL] [Abstract][Full Text] [Related]
13. 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]
14. 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]
15. 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]
16. p.L1612P, a novel voltage-gated sodium channel Nav1.7 mutation inducing a cold sensitive paroxysmal extreme pain disorder.
Suter MR; Bhuiyan ZA; Laedermann CJ; Kuntzer T; Schaller M; Stauffacher MW; Roulet E; Abriel H; Decosterd I; Wider C
Anesthesiology; 2015 Feb; 122(2):414-23. PubMed ID: 25285947
[TBL] [Abstract][Full Text] [Related]
17. Phosphorylation of a chronic pain mutation in the voltage-gated sodium channel Nav1.7 increases voltage sensitivity.
Kerth CM; Hautvast P; Körner J; Lampert A; Meents JE
J Biol Chem; 2021; 296():100227. PubMed ID: 33361158
[TBL] [Abstract][Full Text] [Related]
18. [Pain and analgesia : Mutations of voltage-gated sodium channels].
Eberhardt MJ; Leffler A
Schmerz; 2017 Feb; 31(1):14-22. PubMed ID: 27402262
[TBL] [Abstract][Full Text] [Related]
19. Seven novel modulators of the analgesic target NaV 1.7 uncovered using a high-throughput venom-based discovery approach.
Klint JK; Smith JJ; Vetter I; Rupasinghe DB; Er SY; Senff S; Herzig V; Mobli M; Lewis RJ; Bosmans F; King GF
Br J Pharmacol; 2015 May; 172(10):2445-58. PubMed ID: 25754331
[TBL] [Abstract][Full Text] [Related]
20. Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navbeta4 peptide-mediated resurgent sodium currents.
Theile JW; Jarecki BW; Piekarz AD; Cummins TR
J Physiol; 2011 Feb; 589(Pt 3):597-608. PubMed ID: 21115638
[TBL] [Abstract][Full Text] [Related]
[Next] [New Search]