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Research Associate 2 MS
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Research at a Glance
Yale Co-Authors
Frequent collaborators of Shujun Liu's published research.
Publications Timeline
A big-picture view of Shujun Liu's research output by year.
Stephen Waxman, MD, PhD
Sulayman Dib-Hajj, PhD
Grant Higerd-Rusli, PhD, MD
Sidharth Tyagi, PhD
Peng Zhao, PhD
Matthew Alsaloum, PhD
37Publications
1,332Citations
Publications
2024
Real-time imaging of axonal membrane protein life cycles
Tyagi S, Higerd-Rusli G, Akin E, Baker C, Liu S, Dib-Hajj F, Waxman S, Dib-Hajj S. Real-time imaging of axonal membrane protein life cycles. Nature Protocols 2024, 19: 2771-2802. PMID: 38831222, DOI: 10.1038/s41596-024-00997-x.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsAltmetricConceptsMembrane proteinsRecycling of membrane proteinsProtein subcellular localizationMembrane protein homeostasisMembrane protein traffickingEngineered membrane proteinsMultiple membrane proteinsSelf-labeling tagsCell culturesProtein traffickingProtein tagsSubcellular localizationProtein homeostasisSpatiotemporal regulationCellular processesMultiple proteinsSubcellular distributionVesicular packagingThroughput mannerProteinNeuronal compartmentsDistal axonsProtein spatial organizationFluorescent labelingNeuronal culturesCompartment-specific regulation of NaV1.7 in sensory neurons after acute exposure to TNF-α
Tyagi S, Higerd-Rusli G, Ghovanloo M, Dib-Hajj F, Zhao P, Liu S, Kim D, Shim J, Park K, Waxman S, Choi J, Dib-Hajj S. Compartment-specific regulation of NaV1.7 in sensory neurons after acute exposure to TNF-α. Cell Reports 2024, 43: 113685. PMID: 38261513, PMCID: PMC10947185, DOI: 10.1016/j.celrep.2024.113685.Peer-Reviewed Original ResearchCitationsAltmetricConceptsTNF-aSensory neuronsEffect of TNF-aSensory neuron excitabilityTumor necrosis factor-aRegulation of NaV1.7Voltage-gated sodiumPro-inflammatory cytokinesCompartment-specific effectsNeuronal plasma membraneSensitize nociceptorsNeuronal excitabilitySomatic membraneChannel N terminusElectrophysiological recordingsP38 MAPKIon channelsFactor AAcute exposureMolecular determinantsNeuronsAxonal endingsPhospho-acceptor sitesPlasma membraneCompartment-specific regulation
2023
Ih current stabilizes excitability in rodent DRG neurons and reverses hyperexcitability in a nociceptive neuron model of inherited neuropathic pain
Vasylyev D, Liu S, Waxman S. Ih current stabilizes excitability in rodent DRG neurons and reverses hyperexcitability in a nociceptive neuron model of inherited neuropathic pain. The Journal Of Physiology 2023, 601: 5341-5366. PMID: 37846879, PMCID: PMC10843455, DOI: 10.1113/jp284999.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsFunction Nav1.7 mutationsDorsal root ganglion neuronsSmall DRG neuronsDRG neuronsNav1.7 mutationNeuropathic painGanglion neuronsHuman genetic modelsAction potentialsDRG neuron excitabilityDRG neuron hyperexcitabilityRodent DRG neuronsAP generationCardiac cellsPotential molecular targetsNeuron hyperexcitabilitySevere painPain therapeuticsCNS neuronsExcessive firingNeuron excitabilityCentral neuronsSubthreshold oscillationsHyperexcitabilityNeuronal firingConserved but not critical: Trafficking and function of NaV1.7 are independent of highly conserved polybasic motifs
Tyagi S, Sarveswaran N, Higerd-Rusli G, Liu S, Dib-Hajj F, Waxman S, Dib-Hajj S. Conserved but not critical: Trafficking and function of NaV1.7 are independent of highly conserved polybasic motifs. Frontiers In Molecular Neuroscience 2023, 16: 1161028. PMID: 37008789, PMCID: PMC10060856, DOI: 10.3389/fnmol.2023.1161028.Peer-Reviewed Original ResearchCitationsAltmetricConceptsSensory axonsPeripheral voltage-gated sodium channelsMajor unmet clinical needFunction of Nav1.7Non-addictive treatmentsUnmet clinical needVoltage-clamp recordingsVoltage-gated sodium channelsPain therapyChronic painPrimary afferentsNoxious stimuliTherapeutic modalitiesAction potentialsAxonal transportClinical needVesicular packagingSodium channelsHuman painPainAxonal traffickingAxonal surfaceAxonal membraneAxonsAttractive targetInflammation differentially controls transport of depolarizing Nav versus hyperpolarizing Kv channels to drive rat nociceptor activity
Higerd-Rusli G, Tyagi S, Baker C, Liu S, Dib-Hajj F, Dib-Hajj S, Waxman S. Inflammation differentially controls transport of depolarizing Nav versus hyperpolarizing Kv channels to drive rat nociceptor activity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2023, 120: e2215417120. PMID: 36897973, PMCID: PMC10089179, DOI: 10.1073/pnas.2215417120.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCell biological mechanismsAxonal surfaceLive-cell imagingIon channel traffickingAnterograde transport vesiclesTransport vesiclesInflammatory mediatorsChannel traffickingPlasma membraneVesicular loadingIon channelsKv channelsPotential therapeutic targetPotassium channel KSodium channel NaTraffickingBiological mechanismsTherapeutic targetAbundanceRetrograde transportDistal axonsChannel NaInflammatory painNociceptor activityAxonal transportKv7-specific activators hyperpolarize resting membrane potential and modulate human iPSC-derived sensory neuron excitability
Estacion M, Liu S, Cheng X, Dib-Hajj S, Waxman S. Kv7-specific activators hyperpolarize resting membrane potential and modulate human iPSC-derived sensory neuron excitability. Frontiers In Pharmacology 2023, 14: 1138556. PMID: 36923357, PMCID: PMC10008904, DOI: 10.3389/fphar.2023.1138556.Peer-Reviewed Original ResearchCitationsAltmetricPaclitaxel effects on axonal localization and vesicular trafficking of NaV1.8
Baker C, Tyagi S, Higerd-Rusli G, Liu S, Zhao P, Dib-Hajj F, Waxman S, Dib-Hajj S. Paclitaxel effects on axonal localization and vesicular trafficking of NaV1.8. Frontiers In Molecular Neuroscience 2023, 16: 1130123. PMID: 36860665, PMCID: PMC9970094, DOI: 10.3389/fnmol.2023.1130123.Peer-Reviewed Original ResearchCitationsAltmetricConceptsChemotherapy-induced peripheral neuropathyDorsal root gangliaPTX treatmentDRG axonsEffect of paclitaxelVoltage-gated sodium channel NaPain syndromePeripheral neuropathyDRG neuronsSodium channel NaRoot gangliaCell cycle arrestNeuronal somataSensory neuronsSide effectsTherapeutic targetingTumor growthPaclitaxel effectAntineoplastic agentsAxonal localizationPaclitaxelNumber of NaAxonal compartmentAxonsChannel Na
2022
The fates of internalized NaV1.7 channels in sensory neurons: Retrograde cotransport with other ion channels, axon-specific recycling, and degradation
Higerd-Rusli G, Tyagi S, Liu S, Dib-Hajj F, Waxman S, Dib-Hajj S. The fates of internalized NaV1.7 channels in sensory neurons: Retrograde cotransport with other ion channels, axon-specific recycling, and degradation. Journal Of Biological Chemistry 2022, 299: 102816. PMID: 36539035, PMCID: PMC9843449, DOI: 10.1016/j.jbc.2022.102816.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMembrane proteinsIon channelsNeuronal functionDistinct neuronal compartmentsAxonal membrane proteinsRetrograde traffickingNeuronal polarityRecycling pathwayLate endosomesPlasma membraneSpecific proteinsAxonal traffickingNovel mechanismCell membraneSodium channel NaNeuronal compartmentsMultiple pathwaysLive neuronsVoltage-gated sodium channel NaProteinEndocytosisMembrane specializationsTraffickingMembraneChannel NaDepolarizing NaV and Hyperpolarizing KV Channels Are Co-Trafficked in Sensory Neurons
Higerd-Rusli GP, Alsaloum M, Tyagi S, Sarveswaran N, Estacion M, Akin EJ, Dib-Hajj FB, Liu S, Sosniak D, Zhao P, Dib-Hajj SD, Waxman SG. Depolarizing NaV and Hyperpolarizing KV Channels Are Co-Trafficked in Sensory Neurons. Journal Of Neuroscience 2022, 42: 4794-4811. PMID: 35589395, PMCID: PMC9188389, DOI: 10.1523/jneurosci.0058-22.2022.Peer-Reviewed Original ResearchCitationsAltmetricConceptsIon channel traffickingMembrane proteinsChannel traffickingAxonal membrane proteinsTransport vesiclesPhysiological functionsSame vesiclesAxonal proteinsSpecific transport vesiclesIon channelsTrafficking of NaDiverse physiological functionsExcitability disordersDifferent physiological functionsDistinct ion channelsSensory neuron membraneSensory neuronsDistinct functional classesDistinct functional rolesNormal neuronal excitabilityTrafficking mechanismsNeuronal excitabilityPlasma membraneTherapeutic strategiesPrecise regulationStem cell-derived sensory neurons modelling inherited erythromelalgia: normalization of excitability
Alsaloum M, Labau JIR, Liu S, Effraim P, Waxman SG. Stem cell-derived sensory neurons modelling inherited erythromelalgia: normalization of excitability. Brain 2022, 146: 359-371. PMID: 35088838, PMCID: PMC10060693, DOI: 10.1093/brain/awac031.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSensory neuronsPluripotent stem cell-derived sensory neuronsDynamic clamp electrophysiologyMediators of painUnmet healthcare needsEffective therapeutic approachErythromelalgia mutationAmeliorate painNeuronal hyperexcitabilityPain disordersClinical studiesNeuronal excitabilityPreclinical studiesTherapeutic approachesEffective treatmentNaV1.7 currentsBaseline levelsClamp electrophysiologyHealthcare needsNav1.7 channelsPainErythromelalgiaHyperexcitabilityFunction mutationsNav1.7
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