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The Journal of Physiology|December 2, 2017
Using voltage-sensor toxins and their molecular targets to investigate Na<sub>V</sub> 1.8 gatingJohn Gilchrist, Frank BosmansToxins|September 27, 2012
Animal toxins can alter the function of Nav1.8 and Nav1.9John Gilchrist, Frank BosmansHandbook of Experimental Pharmacology|April 17, 2014
Animal toxins influence voltage-gated sodium channel functionJohn Gilchrist, Baldomero M Olivera, Frank BosmansElife|February 20, 2016
Binary architecture of the Nav1.2-β2 signaling complexSamir Das, John Gilchrist, Frank Bosmans, et al.Proceedings of the National Academy of Sciences of the United States of America|December 4, 2013
Crystallographic insights into sodium-channel modulation by the β4 subunitJohn Gilchrist, Samir Das, Filip Van Petegem, et al.Nature Communications|July 12, 2014
A distinct sodium channel voltage-sensor locus determines insect selectivity of the spider toxin Dc1aNiraj S Bende, Sławomir Dziemborowicz, Mehdi Mobli, et al.Biochemical Pharmacology|June 9, 2020
Mutational analysis of ProTx-I and the novel venom peptide Pe1b provide insight into residues responsible for selective inhibition of the analgesic drug target Na<sub>V</sub>1.7Darshani B Rupasinghe, Volker Herzig, Irina Vetter, et al.Scientific Reports|July 8, 2016
Molecular basis of the remarkable species selectivity of an insecticidal sodium channel toxin from the African spider Augacephalus ezendamiVolker Herzig, Maria Ikonomopoulou, Jennifer J Smith, et al.Toxicon : Official Journal of the International Society on Toxinology|October 30, 2016
Isolation of two insecticidal toxins from venom of the Australian theraphosid spider Coremiocnemis tropixMaria P Ikonomopoulou, Jennifer J Smith, Volker Herzig, et al.JCI Insight|June 8, 2018
NaV1.1 inhibition can reduce visceral hypersensitivityJuan Salvatierra, Joel Castro, Andelain Erickson, et al.Pageof 2