2019
Targeting of dermal myofibroblasts through death receptor 5 arrests fibrosis in mouse models of scleroderma
Park J, Oh Y, Park Y, Park O, Yang H, Slania S, Hummers L, Shah A, An H, Jang J, Horton M, Shin J, Dietz H, Song E, Na D, Park E, Kim K, Lee K, Roschke V, Hanes J, Pomper M, Lee S. Targeting of dermal myofibroblasts through death receptor 5 arrests fibrosis in mouse models of scleroderma. Nature Communications 2019, 10: 1128. PMID: 30850660, PMCID: PMC6408468, DOI: 10.1038/s41467-019-09101-4.Peer-Reviewed Original ResearchMeSH KeywordsActinsAdultAgedAnimalsApoptosisCell DifferentiationCollagenDermisDisease Models, AnimalFemaleFibroblastsFibrosisGene Expression RegulationHumansMaleMiceMiddle AgedMolecular Targeted TherapyMyofibroblastsProtein EngineeringReceptors, TNF-Related Apoptosis-Inducing LigandScleroderma, SystemicSignal TransductionTNF-Related Apoptosis-Inducing LigandConceptsMouse modelAutoimmune rheumatic disordersΑ-smooth muscle actinDeath receptorsAnti-fibrotic effectsMajor therapeutic targetNormal skin architectureDeath receptor 5Upregulated DR5Cognate death receptorsApoptosis-inducing ligandScleroderma progressionRheumatic disordersSevere fibrosisSkin fibrosisViable therapyReceptor 5Therapeutic targetTRAIL pathwayResident fibroblastsSclerodermaFibrogenic componentsFibrosisMuscle actinMyofibroblasts
2011
Characterization of HCV Interactions with Toll-Like Receptors and RIG-I in Liver Cells
Eksioglu E, Zhu H, Bayouth L, Bess J, Liu H, Nelson D, Liu C. Characterization of HCV Interactions with Toll-Like Receptors and RIG-I in Liver Cells. PLOS ONE 2011, 6: e21186. PMID: 21695051, PMCID: PMC3117876, DOI: 10.1371/journal.pone.0021186.Peer-Reviewed Original ResearchMeSH KeywordsCell DeathCell Line, TumorDEAD Box Protein 58DEAD-box RNA HelicasesDown-RegulationHepacivirusHost-Pathogen InteractionsHumansInterferon-betaLiverProtein BindingReceptors, ImmunologicSignal TransductionTNF-Related Apoptosis-Inducing LigandToll-Like ReceptorsViral Envelope ProteinsVirus ReplicationConceptsHuh7.5 cellsViral replicationHCV chronic patientsExpression of TLR3Toll-like receptorsHCV envelope proteinsExpression levelsRIG-I expressionHCV interactionChronic patientsHCVTRAIL pathwayViral escapeViral infectionInnate immunityViral pathogenesisTLR3Induction of apoptosisAntiviral stateIFN inductionLow expression levelsLiver cellsLH86Envelope proteinIFN
2010
Recurrence‐free survival in prostate cancer is related to increased stromal TRAIL expression
Anees M, Horak P, El‐Gazzar A, Susani M, Heinze G, Perco P, Loda M, Lis R, Krainer M, Oh W. Recurrence‐free survival in prostate cancer is related to increased stromal TRAIL expression. Cancer 2010, 117: 1172-1182. PMID: 21381010, DOI: 10.1002/cncr.25504.Peer-Reviewed Original ResearchConceptsRecurrence-free survivalProstate cancer patientsTRAIL expressionProstate cancerExpression of TRAILTumor microenvironmentTissue microarrayTRAIL pathwayCancer patientsDecoy receptorRecurrence-free survival ratesDeath receptorsStromal tumor microenvironmentTumor immune surveillanceProstate cancer epitheliumMultiple tumor typesProstate cancer tissuesOverall survivalFLICE-inhibitory proteinEpithelial expressionOvarian cancerCancer epitheliumClinicopathological parametersImmune surveillanceImpact cancer survival
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