Sodium channel, Neuroscience, Dorsal root ganglion, Paroxysmal extreme pain disorder and Nav1.9 are his primary areas of study. Sulayman D. Dib-Hajj studies Sodium channel, namely NAV1. His Neuroscience research integrates issues from Biophysics, Nociceptor and Ion channel.
His Dorsal root ganglion research incorporates elements of Anesthesia, Nociception, Molecular biology, Bursting and Tetrodotoxin. The study incorporates disciplines such as Sodium channel blocker, Erythromelalgia, Chronic pain and Neuropathic pain in addition to Paroxysmal extreme pain disorder. His Nav1.9 research incorporates themes from Membrane potential and Anatomy.
Sulayman D. Dib-Hajj mainly focuses on Sodium channel, Neuroscience, Dorsal root ganglion, Erythromelalgia and NAV1. His studies deal with areas such as Mutation, Nav1.9, Patch clamp and Cell biology as well as Sodium channel. His Mutation study combines topics from a wide range of disciplines, such as Peripheral neuropathy and Mutant.
The study of Neuroscience is intertwined with the study of Nociceptor in a number of ways. Sulayman D. Dib-Hajj usually deals with Dorsal root ganglion and limits it to topics linked to Neuropathic pain and Carbamazepine. His Erythromelalgia research is multidisciplinary, incorporating elements of Sodium channel blocker and Channelopathy, Internal medicine, Sympathetic ganglion.
His primary scientific interests are in Sodium channel, Neuroscience, Dorsal root ganglion, Neuropathic pain and Chronic pain. His Sodium channel study focuses on NAV1 in particular. Sulayman D. Dib-Hajj regularly ties together related areas like Nav1.9 in his Neuroscience studies.
His Dorsal root ganglion research is multidisciplinary, incorporating perspectives in Peripheral neuropathy, Mutation, Channelopathy, Trigeminal ganglion and Pharmacology. Sulayman D. Dib-Hajj combines subjects such as Electrophysiology and Mutant with his study of Mutation. His study in Chronic pain is interdisciplinary in nature, drawing from both Anesthesia, Erythromelalgia, Pharmacotherapy and Bioinformatics.
His main research concerns Neuroscience, Sodium channel, Chronic pain, Dorsal root ganglion and Erythromelalgia. His Neuroscience research incorporates elements of Mutation and Nav1.9. His Sodium channel study incorporates themes from Nociceptor, Patch clamp and Membrane potential.
He interconnects Peripheral nervous system, Anesthesia, Pharmacotherapy and Pharmacogenomics in the investigation of issues within Chronic pain. His Dorsal root ganglion study integrates concerns from other disciplines, such as Neuropathic pain, Denervation, Mutant, Pathology and Intracellular. Sulayman D. Dib-Hajj has included themes like Paroxysmal extreme pain disorder, Genetic model and Bioinformatics in his Erythromelalgia study.
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NaN, a novel voltage-gated Na channel, is expressed preferentially in peripheral sensory neurons and down-regulated after axotomy
S. D. Dib-Hajj;L. Tyrrell;J. A. Black;S. G. Waxman.
Proceedings of the National Academy of Sciences of the United States of America (1998)
Sodium Channels in Normal and Pathological Pain
Sulayman D. Dib-Hajj;Theodore R. Cummins;Joel A. Black;Stephen G. Waxman.
Annual Review of Neuroscience (2010)
Spinal sensory neurons express multiple sodium channel α-subunit mRNAs
J.A Black;S Dib-Hajj;S Dib-Hajj;K McNabola;K McNabola;S Jeste;S Jeste.
Molecular Brain Research (1996)
The Na(V)1.7 sodium channel: from molecule to man.
Sulayman D. Dib-Hajj;Yang Yang;Yang Yang;Joel A. Black;Joel A. Black;Stephen G. Waxman;Stephen G. Waxman.
Nature Reviews Neuroscience (2013)
A novel persistent tetrodotoxin-resistant sodium current in SNS-null and wild-type small primary sensory neurons.
Theodore R. Cummins;Sulayman D. Dib-Hajj;Joel A. Black;Armen N. Akopian.
The Journal of Neuroscience (1999)
Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy
Catharina G. Faber;Janneke G.J. Hoeijmakers;Hye Sook Ahn;Hye Sook Ahn;Xiaoyang Cheng;Xiaoyang Cheng.
Annals of Neurology (2012)
Sodium channel α-subunit mRNAs I, II, III, NaG, Na6 and hNE (PN1): Different expression patterns in developing rat nervous system
P.A. Felts;S. Yokoyama;S. Yokoyama;S. Yokoyama;S. Dib-Hajj;S. Dib-Hajj;J.A. Black;J.A. Black.
Molecular Brain Research (1997)
Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons
Sulayman D. Dib-Hajj;Anthony M. Rush;Anthony M. Rush;Theodore Cummins;F. M. Hisama.
A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons
Anthony M. Rush;Sulayman D. Dib-Hajj;Sulayman D. Dib-Hajj;Shujun Liu;Shujun Liu;Theodore R. Cummins.
Proceedings of the National Academy of Sciences of the United States of America (2006)
Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy
Theodore R. Cummins;Sulayman D. Dib-Hajj;Sulayman D. Dib-Hajj;Stephen G. Waxman;Stephen G. Waxman.
The Journal of Neuroscience (2004)
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