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Pain|November 24, 1999
Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic painSulayman D Dib-Hajj, Jenny Fjell, Theodore R Cummins, et al.
Neurology|January 29, 2003
The pentapeptide QYNAD does not block voltage-gated sodium channelsT R Cummins, M Renganathan, P K Stys, et al.
Molecular Psychiatry|August 31, 2011
Dopamine transporter genotype predicts behavioural and neural measures of response inhibitionT D R Cummins, Z Hawi, J Hocking, et al.
Brain : a Journal of Neurology|June 17, 2005
Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neuronsS D Dib-Hajj, A M Rush, T R Cummins, et al.
Journal of Clinical and Translational Science|January 17, 2024
Decentralized research technology use in multicenter clinical research studies based at U.S. academic research centersMollie R Cummins, Jeri Burr, Lisa Young, et al.
Molecular Pain|September 23, 2008
Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitableSulayman D Dib-Hajj, Mark Estacion, Brian W Jarecki, et al.
Frontiers in Cellular Neuroscience|June 29, 2019
Hedgehog Pathway Activation Alters Ciliary Signaling in Primary Hypothalamic CulturesRuchi Bansal, Staci E Engle, Patrick J Antonellis, et al.
The Journal of Biological Chemistry|April 20, 2012
Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates cardiac sodium channel NaV1.5 gating by multiple phosphorylation sitesNicole M Ashpole, Anthony W Herren, Kenneth S Ginsburg, et al.
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