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Items: 1 to 20 of 94

1.

Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(V)1.7 mutant channel.

Yang Y, Dib-Hajj SD, Zhang J, Zhang Y, Tyrrell L, Estacion M, Waxman SG.

Nat Commun. 2012;3:1186. doi: 10.1038/ncomms2184.

2.

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

Fischer TZ, Gilmore ES, Estacion M, Eastman E, Taylor S, Melanson M, Dib-Hajj SD, Waxman SG.

Ann Neurol. 2009 Jun;65(6):733-41. doi: 10.1002/ana.21678.

3.

Deletion mutation of sodium channel Na(V)1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability.

Cheng X, Dib-Hajj SD, Tyrrell L, Te Morsche RH, Drenth JP, Waxman SG.

Brain. 2011 Jul;134(Pt 7):1972-86. doi: 10.1093/brain/awr143.

4.

Molecular architecture of a sodium channel S6 helix: radial tuning of the voltage-gated sodium channel 1.7 activation gate.

Yang Y, Estacion M, Dib-Hajj SD, Waxman SG.

J Biol Chem. 2013 May 10;288(19):13741-7. doi: 10.1074/jbc.M113.462366. Epub 2013 Mar 27.

5.

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. doi: 10.1152/jn.00763.2013. Epub 2014 Jan 8.

6.

Depolarized inactivation overcomes impaired activation to produce DRG neuron hyperexcitability in a Nav1.7 mutation in a patient with distal limb pain.

Huang J, Yang Y, Dib-Hajj SD, van Es M, Zhao P, Salomon J, Drenth JP, Waxman SG.

J Neurosci. 2014 Sep 10;34(37):12328-40. doi: 10.1523/JNEUROSCI.2773-14.2014.

7.

The Na(V)1.7 sodium channel: from molecule to man.

Dib-Hajj SD, Yang Y, Black JA, Waxman SG.

Nat Rev Neurosci. 2013 Jan;14(1):49-62. doi: 10.1038/nrn3404. Epub 2012 Dec 12. Review.

PMID:
23232607
8.

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. doi: 10.1124/mol.111.072751. Epub 2011 Jul 25.

9.

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 22;28(43):11079-88. doi: 10.1523/JNEUROSCI.3443-08.2008.

10.

Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons.

Harty TP, Dib-Hajj SD, Tyrrell L, Blackman R, Hisama FM, Rose JB, Waxman SG.

J Neurosci. 2006 Nov 29;26(48):12566-75.

11.

Size matters: Erythromelalgia mutation S241T in Nav1.7 alters channel gating.

Lampert A, Dib-Hajj SD, Tyrrell L, Waxman SG.

J Biol Chem. 2006 Nov 24;281(47):36029-35. Epub 2006 Sep 28.

12.

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 24;289(4):1971-80. doi: 10.1074/jbc.M113.502211. Epub 2013 Dec 5.

13.

A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity.

Sheets PL, Jackson JO 2nd, Waxman SG, Dib-Hajj SD, Cummins TR.

J Physiol. 2007 Jun 15;581(Pt 3):1019-31. Epub 2007 Apr 12.

14.

Familial pain syndromes from mutations of the NaV1.7 sodium channel.

Fischer TZ, Waxman SG.

Ann N Y Acad Sci. 2010 Jan;1184:196-207. doi: 10.1111/j.1749-6632.2009.05110.x. Review.

PMID:
20146699
15.

A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat.

Jarvis MF, Honore P, Shieh CC, Chapman M, Joshi S, Zhang XF, Kort M, Carroll W, Marron B, Atkinson R, Thomas J, Liu D, Krambis M, Liu Y, McGaraughty S, Chu K, Roeloffs R, Zhong C, Mikusa JP, Hernandez G, Gauvin D, Wade C, Zhu C, Pai M, Scanio M, Shi L, Drizin I, Gregg R, Matulenko M, Hakeem A, Gross M, Johnson M, Marsh K, Wagoner PK, Sullivan JP, Faltynek CR, Krafte DS.

Proc Natl Acad Sci U S A. 2007 May 15;104(20):8520-5. Epub 2007 May 2.

16.

Erythromelalgia mutation Q875E Stabilizes the activated state of sodium channel Nav1.7.

Stadler T, O'Reilly AO, Lampert A.

J Biol Chem. 2015 Mar 6;290(10):6316-25. doi: 10.1074/jbc.M114.605899. Epub 2015 Jan 9.

PMID:
25575597
17.

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 20;35(20):7674-81. doi: 10.1523/JNEUROSCI.3935-14.2015.

18.

Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated protein kinase increases current density in dorsal root ganglion neurons.

Hudmon A, Choi JS, Tyrrell L, Black JA, Rush AM, Waxman SG, Dib-Hajj SD.

J Neurosci. 2008 Mar 19;28(12):3190-201. doi: 10.1523/JNEUROSCI.4403-07.2008.

19.

Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7.

Estacion M, Han C, Choi JS, Hoeijmakers JG, Lauria G, Drenth JP, Gerrits MM, Dib-Hajj SD, Faber CG, Merkies IS, Waxman SG.

Mol Pain. 2011 Dec 2;7:92. doi: 10.1186/1744-8069-7-92.

20.

Voltage-gated sodium channels: therapeutic targets for pain.

Dib-Hajj SD, Black JA, Waxman SG.

Pain Med. 2009 Oct;10(7):1260-9. doi: 10.1111/j.1526-4637.2009.00719.x. Review.

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