2007
A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity
Sheets PL, Jackson JO, Waxman SG, Dib‐Hajj S, Cummins TR. A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity. The Journal Of Physiology 2007, 581: 1019-1031. PMID: 17430993, PMCID: PMC2170829, DOI: 10.1113/jphysiol.2006.127027.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnesthetics, LocalBinding SitesCell LineComputer SimulationDose-Response Relationship, DrugErythromelalgiaGanglia, SpinalHumansIon Channel GatingKineticsLidocaineModels, NeurologicalMutationNAV1.7 Voltage-Gated Sodium ChannelNerve Tissue ProteinsNeurons, AfferentSodium Channel BlockersSodium ChannelsTransfectionVoltage-Gated Sodium Channel beta-2 SubunitConceptsErythromelalgia mutationLidocaine inhibitionLocal anesthetic binding siteLocal anestheticsK mutationWild-type Nav1.7Use-dependent inhibitionSlow inactivationSteady-state slow inactivationAnesthetic binding sitesLidocaine sensitivityNeuronal hyperexcitabilityLidocaine treatmentSensory neuronsNaV1.7 currentsErythromelalgiaLidocaineNav1.7Electrophysiological differencesInhibitory effectChannel mutationsSodium channelsHyperexcitabilityK channelsAnesthetics
1997
TTX-Sensitive and -Resistant Na+ Currents, and mRNA for the TTX-Resistant rH1 Channel, Are Expressed in B104 Neuroblastoma Cells
Gu X, Dib-Hajj S, Rizzo M, Waxman S. TTX-Sensitive and -Resistant Na+ Currents, and mRNA for the TTX-Resistant rH1 Channel, Are Expressed in B104 Neuroblastoma Cells. Journal Of Neurophysiology 1997, 77: 236-246. PMID: 9120565, DOI: 10.1152/jn.1997.77.1.236.Peer-Reviewed Original ResearchConceptsB104 neuroblastoma cellsTTX-resistant channelsB104 cellsNeuroblastoma cellsWhole-cell patch-clamp methodAbsence of TTXTTX-resistant currentTTX-sensitive currentsPresence of TTXPA/pFTranscription-polymerase chain reactionLong QT syndromeCell linesSteady-state inactivationNeuroblastoma cell linesAlpha-subunit mRNAPatch-clamp methodTTX-sensitiveHalf-maximal inhibitionInactivation time constantsChannel mRNATTXMembrane excitabilitySubunit mRNAsRT-PCR
1995
A UV-induced, Mg(2+)-dependent crosslink traps an active form of domain 3 of a self-splicing group II intron.
Podar M, Dib-Hajj S, Perlman P. A UV-induced, Mg(2+)-dependent crosslink traps an active form of domain 3 of a self-splicing group II intron. RNA 1995, 1: 828-40. PMID: 7493328, PMCID: PMC1369323.Peer-Reviewed Original Research
1993
Domain 5 interacts with domain 6 and influences the second transesterification reaction of group II intron self-splicing
Dib-Hajj S, Boulanger S, Hebbar S, Peebles C, Franzen J, Perlman P. Domain 5 interacts with domain 6 and influences the second transesterification reaction of group II intron self-splicing. Nucleic Acids Research 1993, 21: 1797-1804. PMID: 8493099, PMCID: PMC309417, DOI: 10.1093/nar/21.8.1797.Peer-Reviewed Original ResearchConceptsSplice site useSplice site utilizationSplice siteDomain 5Yeast mitochondrial DNAGroup II intronsSecond transesterification reactionSubstrate transcriptsCoxI geneSplicing occursMitochondrial DNARNA moleculesDomain 6RNAExonsD5 RNASite utilizationTranscriptsKey roleIntronsBranchingSite residentsSite useGenesSites