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Items: 1 to 20 of 117


A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons.

Rush AM, Dib-Hajj SD, Liu S, Cummins TR, Black JA, Waxman SG.

Proc Natl Acad Sci U S A. 2006 May 23;103(21):8245-50. Epub 2006 May 15.


Differential effect of D623N variant and wild-type Na(v)1.7 sodium channels on resting potential and interspike membrane potential of dorsal root ganglion neurons.

Ahn HS, Vasylyev DV, Estacion M, Macala LJ, Shah P, Faber CG, Merkies IS, Dib-Hajj SD, Waxman SG.

Brain Res. 2013 Sep 5;1529:165-77. doi: 10.1016/j.brainres.2013.07.005. Epub 2013 Jul 11.


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.


The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy.

Han C, Yang Y, de Greef BT, Hoeijmakers JG, Gerrits MM, Verhamme C, Qu J, Lauria G, Merkies IS, Faber CG, Dib-Hajj SD, Waxman SG.

Neuromolecular Med. 2015 Jun;17(2):158-69. doi: 10.1007/s12017-015-8347-9. Epub 2015 Mar 20.


Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable.

Dib-Hajj SD, Estacion M, Jarecki BW, Tyrrell L, Fischer TZ, Lawden M, Cummins TR, Waxman SG.

Mol Pain. 2008 Sep 19;4:37. doi: 10.1186/1744-8069-4-37.


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.


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.


Ca2+ toxicity due to reverse Na+/Ca2+ exchange contributes to degeneration of neurites of DRG neurons induced by a neuropathy-associated Nav1.7 mutation.

Estacion M, Vohra BP, Liu S, Hoeijmakers J, Faber CG, Merkies IS, Lauria G, Black JA, Waxman SG.

J Neurophysiol. 2015 Sep;114(3):1554-64. doi: 10.1152/jn.00195.2015. Epub 2015 Jul 8.


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.


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.


Small-fiber neuropathy Nav1.8 mutation shifts activation to hyperpolarized potentials and increases excitability of dorsal root ganglion neurons.

Huang J, Yang Y, Zhao P, Gerrits MM, Hoeijmakers JG, Bekelaar K, Merkies IS, Faber CG, Dib-Hajj SD, Waxman SG.

J Neurosci. 2013 Aug 28;33(35):14087-97. doi: 10.1523/JNEUROSCI.2710-13.2013.


Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons.

Ahn HS, Black JA, Zhao P, Tyrrell L, Waxman SG, Dib-Hajj SD.

Mol Pain. 2011 May 10;7:32. doi: 10.1186/1744-8069-7-32.


Modulation of peripheral Na(+) channels and neuronal firing by n-butyl-p-aminobenzoate.

Thériault O, Poulin H, Sculptoreanu A, de Groat WC, O'Leary ME, Chahine M.

Eur J Pharmacol. 2014 Mar 15;727:158-66. doi: 10.1016/j.ejphar.2014.01.036. Epub 2014 Jan 30.


Relationship between sodium channel NaV1.3 expression and neuropathic pain behavior in rats.

Lindia JA, Köhler MG, Martin WJ, Abbadie C.

Pain. 2005 Sep;117(1-2):145-53.


Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy.

Han C, Hoeijmakers JG, Liu S, Gerrits MM, te Morsche RH, Lauria G, Dib-Hajj SD, Drenth JP, Faber CG, Merkies IS, Waxman SG.

Brain. 2012 Sep;135(Pt 9):2613-28. doi: 10.1093/brain/aws187. Epub 2012 Jul 22.


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.


Properties of wild-type and fluorescent protein-tagged mouse tetrodotoxin-resistant sodium channel (Na V 1.8) heterologously expressed in rat sympathetic neurons.

Schofield GG, Puhl HL 3rd, Ikeda SR.

J Neurophysiol. 2008 Apr;99(4):1917-27. doi: 10.1152/jn.01170.2007. Epub 2008 Feb 13.


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.

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