2022
FK506-Binding Protein 11 Is a Novel Plasma Cell-Specific Antibody Folding Catalyst with Increased Expression in Idiopathic Pulmonary Fibrosis
Preisendörfer S, Ishikawa Y, Hennen E, Winklmeier S, Schupp JC, Knüppel L, Fernandez IE, Binzenhöfer L, Flatley A, Juan-Guardela BM, Ruppert C, Guenther A, Frankenberger M, Hatz RA, Kneidinger N, Behr J, Feederle R, Schepers A, Hilgendorff A, Kaminski N, Meinl E, Bächinger HP, Eickelberg O, Staab-Weijnitz CA. FK506-Binding Protein 11 Is a Novel Plasma Cell-Specific Antibody Folding Catalyst with Increased Expression in Idiopathic Pulmonary Fibrosis. Cells 2022, 11: 1341. PMID: 35456020, PMCID: PMC9027113, DOI: 10.3390/cells11081341.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPlasma cellsPulmonary fibrosisIgG antibodiesFatal chronic lung diseaseCell linesAntibody-producing plasma cellsChronic lung diseaseAdaptive immune responsesHybridoma cell linesAlveolar epithelial cell lineCell-specific antibodiesCell deathAntibody-producing hybridoma cellsAutoimmune featuresX-box-binding protein 1IPF lungsLung diseaseEpithelial cell lineImmune responseLymphatic tissueB cellsStress-mediated cell deathAntibody secretionER stress-mediated cell death
2020
CMH-Small Molecule Docks into SIRT1, Elicits Human IPF-Lung Fibroblast Cell Death, Inhibits Ku70-deacetylation, FLIP and Experimental Pulmonary Fibrosis
Konikov-Rozenman J, Breuer R, Kaminski N, Wallach-Dayan SB. CMH-Small Molecule Docks into SIRT1, Elicits Human IPF-Lung Fibroblast Cell Death, Inhibits Ku70-deacetylation, FLIP and Experimental Pulmonary Fibrosis. Biomolecules 2020, 10: 997. PMID: 32630842, PMCID: PMC7408087, DOI: 10.3390/biom10070997.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAnimalsBinding SitesCASP8 and FADD-Like Apoptosis Regulating ProteinCell LineCell SurvivalDisease Models, AnimalFibroblastsGene Expression RegulationHumansHydroxamic AcidsIdiopathic Pulmonary FibrosisKu AutoantigenLungMaleMiceMice, Inbred C57BLModels, MolecularMolecular Docking SimulationProtein ConformationProtein StabilitySirtuin 1ConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisFibrotic-lung myofibroblastsProgressive lung diseaseExperimental pulmonary fibrosisFibroblast cell deathLung diseaseLung fibrosisLung sectionsVital organsFlow cytometryFibrosisMyofibroblast resistanceRegenerative capacityFLIP levelsCell survivalCell deathImmunoblotCmHSIRT1Activity inhibitionUseful strategySmall moleculesBleomycinMyofibroblasts
2014
Nrf2 Amplifies Oxidative Stress via Induction of Klf9
Zucker SN, Fink EE, Bagati A, Mannava S, Bianchi-Smiraglia A, Bogner PN, Wawrzyniak JA, Foley C, Leonova KI, Grimm MJ, Moparthy K, Ionov Y, Wang J, Liu S, Sexton S, Kandel ES, Bakin AV, Zhang Y, Kaminski N, Segal BH, Nikiforov MA. Nrf2 Amplifies Oxidative Stress via Induction of Klf9. Molecular Cell 2014, 53: 916-928. PMID: 24613345, PMCID: PMC4049522, DOI: 10.1016/j.molcel.2014.01.033.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesBleomycinCell Line, TumorGene Expression RegulationGenes, ReporterHumansKruppel-Like Transcription FactorsLuciferasesLungMiceNF-E2-Related Factor 2NIH 3T3 CellsOxidative StressPromoter Regions, GeneticProtein BindingPulmonary FibrosisReactive Oxygen SpeciesSignal TransductionConceptsReactive oxygen speciesKey transcriptional regulatorMetabolism of ROSOxidative stressPathogenesis of bleomycinKruppel-like factor 9Thioredoxin reductase 2Subsequent cell deathTranscription factor 2Antioxidant gene expressionUbiquitous regulatorsTranscriptional regulatorsIntracellular reactive oxygen speciesLung injuryFeedforward regulationPulmonary fibrosisGene expressionOxidant injuryROS clearanceCell deathReductase 2Mouse tissuesCultured cellsNF-E2Factor 9