Featured Publications
Stimulation of the hepatoportal nerve plexus with focused ultrasound restores glucose homoeostasis in diabetic mice, rats and swine
Cotero V, Graf J, Miwa H, Hirschstein Z, Qanud K, Huerta TS, Tai N, Ding Y, Jimenez-Cowell K, Tomaio JN, Song W, Devarajan A, Tsaava T, Madhavan R, Wallace K, Loghin E, Morton C, Fan Y, Kao TJ, Akhtar K, Damaraju M, Barenboim L, Maietta T, Ashe J, Tracey KJ, Coleman TR, Di Carlo D, Shin D, Zanos S, Chavan SS, Herzog RI, Puleo C. Stimulation of the hepatoportal nerve plexus with focused ultrasound restores glucose homoeostasis in diabetic mice, rats and swine. Nature Biomedical Engineering 2022, 6: 683-705. PMID: 35361935, PMCID: PMC10127248, DOI: 10.1038/s41551-022-00870-w.Peer-Reviewed Original ResearchConceptsGlucose homeostasisGlucose toleranceNerve plexusAfferent autonomic nervesHyperinsulinemic euglycaemic clampNon-pharmacologic therapiesType 2 diabetesInsulin-resistant diabetesHepatic portal systemAutonomic nervesNerve pathwaysDiabetic miceFocused ultrasound stimulationPeripheral neuronsSensory projectionsIntestinal tissueMetabolic diseasesMulti-omics profilingPortal systemMetabolic tissuesGlucose availabilityDiabetesSelective activationPlexusUltrasound stimulation
2019
O-GlcNAcase targets pyruvate kinase M2 to regulate tumor growth
Singh JP, Qian K, Lee JS, Zhou J, Han X, Zhang B, Ong Q, Ni W, Jiang M, Ruan HB, Li MD, Zhang K, Ding Z, Lee P, Singh K, Wu J, Herzog RI, Kaech S, Wendel HG, Yates JR, Han W, Sherwin RS, Nie Y, Yang X. O-GlcNAcase targets pyruvate kinase M2 to regulate tumor growth. Oncogene 2019, 39: 560-573. PMID: 31501520, PMCID: PMC7107572, DOI: 10.1038/s41388-019-0975-3.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAcetylglucosamineAnimalsAntigens, NeoplasmCarrier ProteinsCell Line, TumorDatasets as TopicDisease ProgressionFemaleGene Expression ProfilingGlycolysisHEK293 CellsHistone AcetyltransferasesHumansHyaluronoglucosaminidaseMaleMembrane ProteinsMiceN-AcetylglucosaminyltransferasesNeoplasm GradingNeoplasm StagingNeoplasmsProtein Processing, Post-TranslationalThyroid HormonesTissue Array AnalysisUp-RegulationXenograft Model Antitumor AssaysConceptsPyruvate kinase M2O-GlcNAcaseAerobic glycolysisO-GlcNAcylationKinase M2Lysine acetyltransferase activityTumor growthMetabolic rheostatAcetyltransferase activityGlcNAc transferaseMolecular basisMetabolic shiftHuman cancersGlycolysisCancer cellsHigh glucose conditionsGlucose availabilityTumor progressionGlucose conditionsExquisite controlGrowthRheostatCausative roleTargetEnzyme
2017
β-Hydroxybutyrate Deactivates Neutrophil NLRP3 Inflammasome to Relieve Gout Flares
Goldberg EL, Asher JL, Molony RD, Shaw AC, Zeiss CJ, Wang C, Morozova-Roche LA, Herzog RI, Iwasaki A, Dixit VD. β-Hydroxybutyrate Deactivates Neutrophil NLRP3 Inflammasome to Relieve Gout Flares. Cell Reports 2017, 18: 2077-2087. PMID: 28249154, PMCID: PMC5527297, DOI: 10.1016/j.celrep.2017.02.004.Peer-Reviewed Original ResearchConceptsKetogenic dietGouty flaresΒ-hydroxybutyrateMajor risk factorAnti-inflammatory moleculesNLRP3-dependent mannerAlternate metabolic fuelsGout flaresJoint destructionIL-1βIntense painInterleukin-1βNLRP3 inflammasomeRisk factorsInflammatory neutrophilsBacterial infectionsNeutrophilsNLRP3Immune defenseGoutMetabolic fuelsBHBS100A9 fibrilsDietPain
2016
Pigment epithelium‐derived factor restoration increases bone mass and improves bone plasticity in a model of osteogenesis imperfecta type VI via Wnt3a blockade
Belinsky GS, Sreekumar B, Andrejecsk JW, Saltzman WM, Gong J, Herzog RI, Lin S, Horsley V, Carpenter TO, Chung C. Pigment epithelium‐derived factor restoration increases bone mass and improves bone plasticity in a model of osteogenesis imperfecta type VI via Wnt3a blockade. The FASEB Journal 2016, 30: 2837-2848. PMID: 27127101, PMCID: PMC4970601, DOI: 10.1096/fj.201500027r.Peer-Reviewed Original ResearchConceptsPigment epithelium-derived factorOsteogenesis imperfecta type VIWnt/β-catenin signalingBone massOI type VIΒ-catenin signalingAbility of PEDFTrabecular bone volume/total volumeType VIBone volume/total volumeWild-type miceEpithelium-derived factorBone plasticityPEDF-knockout miceMesenchymal stem cell commitmentBone volume fractionKO micePEDF peptidesStem cell commitmentFluorescent protein reporterCombination of Wnt3aMouse modelWnt modulatorsBone mineralizationMice
2015
Hyperglycemia repression of miR-24 coordinately upregulates endothelial cell expression and secretion of von Willebrand factor
Xiang Y, Cheng J, Wang D, Hu X, Xie Y, Stitham J, Atteya G, Du J, Tang WH, Lee SH, Leslie K, Spollett G, Liu Z, Herzog E, Herzog RI, Lu J, Martin KA, Hwa J. Hyperglycemia repression of miR-24 coordinately upregulates endothelial cell expression and secretion of von Willebrand factor. Blood 2015, 125: 3377-3387. PMID: 25814526, PMCID: PMC4447857, DOI: 10.1182/blood-2015-01-620278.Peer-Reviewed Original ResearchConceptsVon Willebrand factorDiabetes mellitusMiR-24Diabetic patientsAdverse thrombotic eventsThrombotic cardiovascular eventsVWF expressionWillebrand factorDiabetic mouse modelNovel therapeutic targetHistamine H1 receptorsEndothelial cell expressionHyperglycemia-induced activationCardiovascular eventsThrombotic eventsH1 receptorsMouse modelVWF levelsTherapeutic targetCell expressionMellitusPatientsEndothelial cellsElevated levelsReactive oxygen species
2013
Vaccination with Single Chain Antigen Receptors for Islet-Derived Peptides Presented on I-Ag7 Delays Diabetes in NOD Mice by Inducing Anergy in Self-Reactive T-Cells
Gurr W, Shaw M, Herzog RI, Li Y, Sherwin R. Vaccination with Single Chain Antigen Receptors for Islet-Derived Peptides Presented on I-Ag7 Delays Diabetes in NOD Mice by Inducing Anergy in Self-Reactive T-Cells. PLOS ONE 2013, 8: e69464. PMID: 23894487, PMCID: PMC3722102, DOI: 10.1371/journal.pone.0069464.Peer-Reviewed Original ResearchConceptsSelf-reactive T cellsSingle chain receptorT cellsNOD miceB cellsReceptor repertoireSelf-reactive T cell clonesT cell receptor repertoireAnti-idiotypic vaccinationNormal NOD micePancreatic lymph nodesOnset of T1D.NOD-scid recipientsB cell receptor repertoireType 1 diabetesT cell clonesBDC2.5 TCRNOD recipientsProfound anergyLymph nodesSpecific autoantigensInducer cellsVaccination approachesMHC IVaccination
2005
Nav1.6 channels generate resurgent sodium currents in spinal sensory neurons
Cummins TR, Dib-Hajj SD, Herzog RI, Waxman SG. Nav1.6 channels generate resurgent sodium currents in spinal sensory neurons. FEBS Letters 2005, 579: 2166-2170. PMID: 15811336, DOI: 10.1016/j.febslet.2005.03.009.Peer-Reviewed Original ResearchConceptsResurgent sodium currentsResurgent currentsDRG neuronsLarge-diameter dorsal root ganglion neuronsSodium currentDorsal root ganglion neuronsSmall DRG neuronsSpinal sensory neuronsWild-type miceCerebellar Purkinje neuronsVoltage-gated sodium channelsGanglion neuronsSensory neuronsPurkinje neuronsNull miceNav1.6 channelsNeuronsSodium channelsMiceCell background
2003
Calmodulin Binds to the C Terminus of Sodium Channels Nav1.4 and Nav1.6 and Differentially Modulates Their Functional Properties
Herzog RI, Liu C, Waxman SG, Cummins TR. Calmodulin Binds to the C Terminus of Sodium Channels Nav1.4 and Nav1.6 and Differentially Modulates Their Functional Properties. Journal Of Neuroscience 2003, 23: 8261-8270. PMID: 12967988, PMCID: PMC6740705, DOI: 10.1523/jneurosci.23-23-08261.2003.Peer-Reviewed Original ResearchConceptsVoltage-gated sodium channelsSodium channelsNeuronal sodium channelsCalcium-independent mechanismVGSC isoformsNeuronal plasticityCell excitabilityNav1.6 channelsNav1.6Overexpression of CaMCalcium-dependent mannerCalcium-independent mannerNav1.4Sodium channel Nav1.4Channel Nav1.4Functional expressionCurrent amplitudeDistinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons
Herzog RI, Cummins TR, Ghassemi F, Dib-Hajj SD, Waxman SG. Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons. The Journal Of Physiology 2003, 551: 741-750. PMID: 12843211, PMCID: PMC2343279, DOI: 10.1113/jphysiol.2003.047357.Peer-Reviewed Original ResearchAnesthetics, LocalAnimalsCells, CulturedGanglia, SpinalIon Channel GatingKineticsMiceMice, Mutant StrainsNAV1.6 Voltage-Gated Sodium ChannelNAV1.7 Voltage-Gated Sodium ChannelNAV1.8 Voltage-Gated Sodium ChannelNerve Tissue ProteinsNeurons, AfferentPatch-Clamp TechniquesRecombinant ProteinsSodium ChannelsTetrodotoxinThe pentapeptide QYNAD does not block voltage-gated sodium channels
Cummins TR, Renganathan M, Stys PK, Herzog RI, Scarfo K, Horn R, Dib-Hajj SD, Waxman SG. The pentapeptide QYNAD does not block voltage-gated sodium channels. Neurology 2003, 60: 224-229. PMID: 12552035, DOI: 10.1212/01.wnl.0000042423.36650.bd.Peer-Reviewed Original ResearchConceptsVoltage-gated sodium channelsSodium channelsDifferent sodium channel subtypesSodium currentDorsal root ganglion neuronsInflammatory neurologic disordersMajor sodium channelPatch-clamp recordingsSodium channel subtypesSodium channel functionNodes of RanvierPentapeptide QYNADOptic nerveGanglion neuronsIntact neuronsNeurologic disordersQYNADChannel subtypesHuman CSFAbnormal myelinFiber tractsElevated levelsEndogenous pentapeptideMicro MChannel function
2001
Persistent TTX-Resistant Na+ Current Affects Resting Potential and Response to Depolarization in Simulated Spinal Sensory Neurons
Herzog RI, Cummins TR, Waxman SG. Persistent TTX-Resistant Na+ Current Affects Resting Potential and Response to Depolarization in Simulated Spinal Sensory Neurons. Journal Of Neurophysiology 2001, 86: 1351-1364. PMID: 11535682, DOI: 10.1152/jn.2001.86.3.1351.Peer-Reviewed Original ResearchConceptsPersistent TTX-R currentTTX-R currentsSmall DRG neuronsSodium currentDRG neuronsSmall dorsal root ganglion neuronsTTX-resistant sodium currentsDorsal root ganglion neuronsVoltage-gated sodium currentTetrodotoxin-sensitive sodium currentTTX-S currentsSpinal sensory neuronsGanglion neuronsNeuronal excitabilitySensory neuronsAction potentialsNeuronsSubthreshold stimuliDepolarizing phaseSpike electrogenesisAnode break excitationElectrogenic propertiesBreak excitationPossible contributionInactivation gate