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Annual Review of Neuroscience|February 1, 2019
Sodium Channels in Human Pain Disorders: Genetics and PharmacogenomicsSulayman D Dib-Hajj, Stephen G WaxmanAnnals of Neurology|June 2, 2005
Erythromelalgia: a hereditary pain syndrome enters the molecular eraStephen G Waxman, Sulayman D Dib-HajjNeuroscience Letters|September 7, 2010
Isoform-specific and pan-channel partners regulate trafficking and plasma membrane stability; and alter sodium channel gating propertiesSulayman D Dib-Hajj, Stephen G WaxmanScience Translational Medicine|August 15, 2014
Translational pain research: Lessons from genetics and genomicsSulayman D Dib-Hajj, Stephen G WaxmanThe Journal of Clinical Investigation|July 1, 2024
Disordered but effective: short linear motifs as gene therapy targets for hyperexcitability disordersSulayman D Dib-Hajj, Stephen G WaxmanMolecular Neurobiology|November 14, 2002
Structure of the sodium channel gene SCN11A: evidence for intron-to-exon conversion model and implications for gene evolutionSulayman D Dib-Hajj, Lynda Tyrrell, Stephen G WaxmanAdvances in Genetics|February 3, 2009
Genetics and molecular pathophysiology of Na(v)1.7-related pain syndromesSulayman D Dib-Hajj, Yong Yang, Stephen G WaxmanMolecular Brain|August 9, 2018
Multiple myosin motors interact with sodium/potassium-ATPase alpha 1 subunitsBhagirathi Dash, Sulayman D Dib-Hajj, Stephen G WaxmanMolecular Pain|June 10, 2010
Effects of ranolazine on wild-type and mutant hNav1.7 channels and on DRG neuron excitabilityMark Estacion, Stephen G Waxman, Sulayman D Dib-HajjPageof 41