Longjun Li
Postdoctoral AssociateDownloadHi-Res Photo
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Postdoctoral Associate
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- Mu Lab
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Medical Research Interests
Biomarkers, Tumor; Cell Death
Public Health Interests
Biomarkers; Immunology
ORCID
0009-0005-4797-9353Mu Lab, Urology
Our lab is dedicated to uncovering the molecular mechanisms that drive resistance to targeted and immune therapies in prostate and other cancers.
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Research at a Glance
Publications Timeline
A big-picture view of Longjun Li's research output by year.
10Publications
352Citations
Publications
2024
Balanced regulation of ROS production and inflammasome activation in preventing early development of colorectal cancer
Li L, Xu T, Qi X. Balanced regulation of ROS production and inflammasome activation in preventing early development of colorectal cancer. Immunological Reviews 2024, 329: e13417. PMID: 39523732, DOI: 10.1111/imr.13417.Peer-Reviewed Original ResearchCitationsConceptsRegulation of ROS productionBalanced ROS productionReactive oxygen speciesROS productionColitis-associated colorectal cancerInflammasome activationColorectal cancerInnate immune response to microbial infectionResponse to microbial infectionImmune response to microbial infectionReactive oxygen species sensorSource of ROS productionCell-cell contactNADPH oxidase complexInflammasome activation studiesReactive oxygen species generationASC speck formationBalance regulationCrohn's diseaseSignaling networksROS signalingSusceptibility genesNADPH complexPerinuclear regionSterile insultsCorrection: FTY720 Inhibits MPP+-Induced Microglial Activation by Affecting NLRP3 Inflammasome Activation
Yao S, Li L, Sun X, Hua J, Zhang K, Hao L, Liu L, Shi D, Zhou H. Correction: FTY720 Inhibits MPP+-Induced Microglial Activation by Affecting NLRP3 Inflammasome Activation. Journal Of Neuroimmune Pharmacology 2024, 19: 42. PMID: 39105974, DOI: 10.1007/s11481-024-10137-7.Peer-Reviewed Original ResearchNCF4 attenuates colorectal cancer progression by modulating inflammasome activation and immune surveillance
Li L, Mao R, Yuan S, Xie Q, Meng J, Gu Y, Tan S, Xu X, Gao C, Liu H, Ma C, Man S, Meng X, Xu T, Qi X. NCF4 attenuates colorectal cancer progression by modulating inflammasome activation and immune surveillance. Nature Communications 2024, 15: 5170. PMID: 38886341, PMCID: PMC11183137, DOI: 10.1038/s41467-024-49549-7.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsCARD Signaling Adaptor ProteinsCD8-Positive T-LymphocytesCell Line, TumorColorectal NeoplasmsDisease ProgressionFemaleHumansImmunologic SurveillanceInflammasomesInterleukin-18Killer Cells, NaturalMaleMiceMice, Inbred C57BLMice, KnockoutNADPH OxidasesNLR Family, Pyrin Domain-Containing 3 ProteinPhosphorylationReactive Oxygen SpeciesConceptsInflammasome activationColorectal cancerFive-year survival rateAssociated with colorectal cancer developmentAnti-tumor responsesCD8+ TColorectal cancer developmentColorectal cancer progressionApoptosis-associated speck-like proteinNK cellsImmune surveillanceRegulation of inflammasome activationSpeck-like proteinCancer developmentSurvival rateCancer progressionColorectal tumorigenesisPrecancerous cellsTransit amplifyingAIM2 inflammasome activationImmunoprecipitation-mass spectrometry analysisInflammasome responsesNCF4Modulating inflammasome activationROS levels
2021
Intracellular C3 prevents hepatic steatosis by promoting autophagy and very‐low‐density lipoprotein secretion
Li Y, Sha Y, Wang H, He L, Li L, Wen S, Sheng L, Hu W, Zhou H. Intracellular C3 prevents hepatic steatosis by promoting autophagy and very‐low‐density lipoprotein secretion. The FASEB Journal 2021, 35: e22037. PMID: 34762761, DOI: 10.1096/fj.202100856r.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsVery-low-density lipoprotein secretionVery-low-density lipoproteinProtein disulfide isomeraseExpression of protein disulfide isomeraseMicrosomal TG transfer proteinPathogen recognitionHepatic lipid accumulationDisulfide isomeraseEndoplasmic reticulumIntracellular functionsAutophagy-relatedExtracellular milieuDisrupt interactionsVLDL secretionTransfer proteinLipoprotein secretionLipid accumulationIntracellular C3C3-/- miceComplement component C3C3 knockoutHepatic steatosisConvergence pointWild type miceKnockoutMicroscopic Detection of ASC Inflammasomes in Bone Marrow Derived Macrophages Post Stimulation.
Li L, Mao R, Qi X. Microscopic Detection of ASC Inflammasomes in Bone Marrow Derived Macrophages Post Stimulation. Bio-protocol 2021, 11: e4151. PMID: 34604456, PMCID: PMC8443463, DOI: 10.21769/bioprotoc.4151.Peer-Reviewed Original ResearchCitationsConceptsASC specksAdaptor protein apoptosis-associated speck-like proteinApoptosis-associated speck-like proteinImmunofluorescence cell stainingInflammasome activationSpeck-like proteinStep-by-step protocolASC speck formationPro-caspase-1Multiprotein complexesProtein complexesBacterial pathogensSensor proteinsASC inflammasomeIntracellular localizationASC proteinHost defenseSpeck formationBone marrow-derived macrophagesProteinMarrow-derived macrophagesIntracellular multiprotein complexesInflammasomeConfocal microscopyBMDMsIntravital imaging of interactions between iNKT and kupffer cells to clear free lipids during steatohepatitis
Wang H, Li L, Li Y, Li Y, Sha Y, Wen S, You Q, Liu L, Shi M, Zhou H. Intravital imaging of interactions between iNKT and kupffer cells to clear free lipids during steatohepatitis. Theranostics 2021, 11: 2149-2169. PMID: 33500717, PMCID: PMC7797696, DOI: 10.7150/thno.51369.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsInvariant natural killer TInvariant natural killer T cellsINKT cellsAdoptive transfer of iNKT cellsGenes related to phagocytosisKupffer cellsMethionine-choline-deficientNatural killer TPopulation of innate immune cellsConfocal live imagingTranscriptome sequencingCell clustersInnate immune cellsIFN-g expressionLiver fibrosis developmentKiller TStages of steatohepatitisPotential therapeutic strategyLipid processingDiet-induced steatohepatitisAdoptive transferLiver steatohepatitisIFN-gImmune cellsLipid phagocytosis
2020
HUWE1 mediates inflammasome activation and promotes host defense against bacterial infection
Guo Y, Li L, Xu T, Guo X, Wang C, Li Y, Yang Y, Yang D, Sun B, Zhao X, Shao G, Qi X. HUWE1 mediates inflammasome activation and promotes host defense against bacterial infection. Journal Of Clinical Investigation 2020, 130: 6301-6316. PMID: 33104527, PMCID: PMC7685759, DOI: 10.1172/jci138234.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsApoptosis Regulatory ProteinsBacteriaBacterial InfectionsCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsCaspase 1DNA-Binding ProteinsHEK293 CellsHumansInflammasomesInterleukin-1betaMacrophagesMiceMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinTumor Suppressor ProteinsUbiquitin-Protein LigasesConceptsCaspase-1 activationBone marrow-derived macrophagesE3 ubiquitin ligase HUWE1Inflammasome activationUbiquitin ligase HUWE1K27-linked polyubiquitinationBacterial infectionsMechanisms of inflammasome activationBH3 domainASC speck formationHIN domainCaspase-1 maturationPromote host defenseIncreased bacterial burdenNACHT domain of NLRP3NACHT domainHUWE1Decreased caspase-1 activationAcinetobacter baumannii infectionsInflammasome assemblyInduce NLRP3Human cellsHost defenseSpeck formationAIM2 inflammasome activation
2019
SPHK1 deficiency protects mice from acetaminophen-induced ER stress and mitochondrial permeability transition
Li L, Wang H, Zhang J, Sha Y, Wu F, Wen S, He L, Sheng L, You Q, Shi M, Liu L, Zhou H. SPHK1 deficiency protects mice from acetaminophen-induced ER stress and mitochondrial permeability transition. Cell Death & Differentiation 2019, 27: 1924-1937. PMID: 31827236, PMCID: PMC7244772, DOI: 10.1038/s41418-019-0471-x.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsActivation of activating transcription factor 6Mitochondrial permeability transitionApoptosis signal-regulating kinase 1SphK1 deficiencyER stressPermeability transitionEndoplasmic reticulumLevels of activating transcription factor 4Inhibit mitochondrial permeability transitionTranscription factor 6Transcription of inflammatory genesGlycogen synthase kinase 3bSignal-regulated kinases 1Transcription factor 4Phosphorylation of JNKAcetylation of p65Levels of histone deacetylaseHistone deacetylasesSphingosine-1-PhosphateImpaired phosphorylationKinase 1Factor 2AFactor 6Exogenous S1PSphK1FTY720 Inhibits MPP+-Induced Microglial Activation by Affecting NLRP3 Inflammasome Activation
Yao S, Li L, Sun X, Hua J, Zhang K, Hao L, Liu L, Shi D, Zhou H. FTY720 Inhibits MPP+-Induced Microglial Activation by Affecting NLRP3 Inflammasome Activation. Journal Of Neuroimmune Pharmacology 2019, 14: 478-492. PMID: 31069623, DOI: 10.1007/s11481-019-09843-4.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsAntiparkinson AgentsApoptosisCell LineCorpus StriatumCytokinesDopaminergic NeuronsDrug Evaluation, PreclinicalExploratory BehaviorFingolimod HydrochlorideInflammasomesMaleMiceMice, Inbred C57BLMicrogliaMitochondriaMPTP PoisoningNeuroprotective AgentsNLR Family, Pyrin Domain-Containing 3 ProteinParkinsonian DisordersPars CompactaReactive Oxygen SpeciesRotarod Performance TestSignal TransductionConceptsTherapeutic effects of FTY720Effect of FTY720Therapeutic effectNLRP3 inflammasome activationDopaminergic neuronsMicroglial activationP65 activationInflammasome activationSubcutaneous injection of MPTPMPTP-induced microglial activationIncreased dopamine releaseMPTP-induced behavioral deficitsDamage to dopaminergic neuronsTumor necrosis factor-aAnimal models of PDInjection of MPTPROS generationSubstantia nigra pars compactaDecreased NLRP3 inflammasome activationParkinson's diseaseInterleukin (IL)-6Production of interleukin (IL)-6Degeneration of dopaminergic neuronsLoss of dopaminergic neuronsActivation of microglia
2018
FTY720 attenuates behavioral deficits in a murine model of systemic lupus erythematosus
Shi D, Tian T, Yao S, Cao K, Zhu X, Zhang M, Wen S, Li L, Shi M, Zhou H. FTY720 attenuates behavioral deficits in a murine model of systemic lupus erythematosus. Brain Behavior And Immunity 2018, 70: 293-304. PMID: 29548997, DOI: 10.1016/j.bbi.2018.03.009.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsSystemic lupus erythematosusOral administration of FTY720Administration of FTY720Blood-brain barrierCentral nervous systemDepression-like behaviorLupus erythematosusInduce neuropsychiatric disordersMurine model of systemic lupus erythematosusModel of systemic lupus erythematosusTherapeutic strategiesInfiltration of T cellsEffective new therapeutic strategiesLevels of adhesion moleculesTreated with oral administrationT cell recruitmentLevels of inflammatory cytokinesBehavioral deficitsNeuropsychiatric disordersImpact patient qualityCerebral endothelial cellsExpression levels of adhesion moleculesCorticosteroid administrationAlbumin levelsLymph nodes
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