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Proceedings of the National Academy of Sciences of the United States of America|July 8, 1999
Sodium channels and painS G Waxman, S Dib-Hajj, T R Cummins, et al.Science (New York, N.Y.)|August 17, 2002
Splay fault branching along the Nankai subduction zoneJin-Oh Park, Tetsuro Tsuru, Shuichi Kodaira, et al.Frontiers in Pharmacology|May 2, 2022
Neural Activity Correlates With Behavior Effects of Anti-Seizure Drugs Efficacy Using the Zebrafish Pentylenetetrazol Seizure ModelPatrick C Milder, Agnes S Zybura, Theodore R Cummins, et al.Brain : a Journal of Neurology|June 9, 2016
Aberrant epilepsy-associated mutant Nav1.6 sodium channel activity can be targeted with cannabidiolReesha R Patel, Cindy Barbosa, Tatiana Brustovetsky, et al.Pharmacological Reviews|May 26, 2025
5-HT2A receptors: Pharmacology and functional selectivityBenjamin R Cummins, Gerald B Billac, David E Nichols, et al.Molecular Pharmacology|September 22, 2010
The tarantula toxins ProTx-II and huwentoxin-IV differentially interact with human Nav1.7 voltage sensors to inhibit channel activation and inactivationYucheng Xiao, Kenneth Blumenthal, James O Jackson, et al.FEBS Letters|November 22, 1997
Insertion of a SNS-specific tetrapeptide in S3-S4 linker of D4 accelerates recovery from inactivation of skeletal muscle voltage-gated Na channel mu1 in HEK293 cellsS D Dib-Hajj, K Ishikawa, T R Cummins, et al.The Journal of Physiology|July 5, 2008
Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivationBrian W Jarecki, Patrick L Sheets, James O Jackson, et al.Novartis Foundation Symposium|January 5, 2002
Diverse functions and dynamic expression of neuronal sodium channelsStephen G Waxman, Theodore R Cummins, Joel A Black, et al.Journal of Applied Physiology (Bethesda, Md. : 1985)|July 1, 1991
Developmental changes in neuromuscular transmission in the rat diaphragmJ D Feldman, A R Bazzy, T R Cummins, et al.Pageof 30