Featured Publications
m6A mRNA methylation-directed myeloid cell activation controls progression of NAFLD and obesity
Qin Y, Li B, Arumugam S, Lu Q, Mankash SM, Li J, Sun B, Li J, Flavell RA, Li HB, Ouyang X. m6A mRNA methylation-directed myeloid cell activation controls progression of NAFLD and obesity. Cell Reports 2021, 37: 109968. PMID: 34758326, PMCID: PMC8667589, DOI: 10.1016/j.celrep.2021.109968.Peer-Reviewed Original ResearchConceptsNon-alcoholic fatty liver diseaseProgression of NAFLDLineage-restricted deletionFatty liver diseaseMultiple mRNA transcriptsMyeloid cell activationDiet-induced developmentMethyladenosine (m<sup>6</sup>A) RNA modificationMRNA metabolismProtein methyltransferaseLiver diseaseRNA modificationsCellular stressMetabolic reprogrammingDDIT4 mRNACell activationObesityDifferential expressionMammalian targetMRNA transcriptsSignificant downregulationCytokine stimulationPathway activityMetabolic phenotypeMRNA levels
2019
The Reduced Expression of EOLA1 May Be Related to Refractory Diabetic Foot Ulcer
Wu M, Leng W, Pan H, Lei X, Chen L, Ouyang X, Liang Z. The Reduced Expression of EOLA1 May Be Related to Refractory Diabetic Foot Ulcer. Mediators Of Inflammation 2019, 2019: 6705424. PMID: 31007603, PMCID: PMC6441532, DOI: 10.1155/2019/6705424.Peer-Reviewed Original ResearchConceptsDiabetic foot ulcersCourse of diseaseInterleukin-6Diabetes mellitusFoot ulcersWound groupChronic diabetic foot ulcersChronic wound groupsReduced expressionUncontrolled chronic inflammationRelevant clinical dataExpression of NFResults of immunofluorescenceChronic inflammationInflammatory pathwaysIntractable complicationClinical dataImmunohistochemical stainingRefractory woundsInflammatory regulationInflammationUlcersPatientsAW groupUncontrolled activation
2009
AP-1 Activated by Toll-like Receptors Regulates Expression of IL-23 p19*
Liu W, Ouyang X, Yang J, Liu J, Li Q, Gu Y, Fukata M, Lin T, He JC, Abreu M, Unkeless JC, Mayer L, Xiong H. AP-1 Activated by Toll-like Receptors Regulates Expression of IL-23 p19*. Journal Of Biological Chemistry 2009, 284: 24006-24016. PMID: 19592489, PMCID: PMC2781995, DOI: 10.1074/jbc.m109.025528.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 2AnimalsAutoimmune DiseasesCell LineDendritic CellsGene Expression RegulationInterleukin-10Interleukin-23 Subunit p19LipopolysaccharidesMacrophages, PeritonealMAP Kinase Signaling SystemMiceMice, KnockoutMitogen-Activated Protein Kinase KinasesMutationMyeloid Differentiation Factor 88NF-kappa BProto-Oncogene Proteins c-junResponse ElementsToll-Like Receptor 4Transcription Factor AP-1ConceptsIL-23 p19Toll-like receptorsP19 expressionIL-10-deficient miceNF-kappaBMyD88-dependent Toll-like receptorIL-23 expressionRecombinant IL-10IL-12 familyC-JunWild-type miceAP-1 siteC-Fos bindsAP-1Promoter activationIL-23IL-10Dendritic cellsMyD88 pathwayAutoimmune diseasesImmune responseInflammatory signalsType miceLipopolysaccharide (LPS) stimulationNF-kappaB.