2019
Transcriptional regulatory model of fibrosis progression in the human lung
McDonough JE, Ahangari F, Li Q, Jain S, Verleden SE, Herazo-Maya J, Vukmirovic M, DeIuliis G, Tzouvelekis A, Tanabe N, Chu F, Yan X, Verschakelen J, Homer RJ, Manatakis DV, Zhang J, Ding J, Maes K, De Sadeleer L, Vos R, Neyrinck A, Benos PV, Bar-Joseph Z, Tantin D, Hogg JC, Vanaudenaerde BM, Wuyts WA, Kaminski N. Transcriptional regulatory model of fibrosis progression in the human lung. JCI Insight 2019, 4 PMID: 31600171, PMCID: PMC6948862, DOI: 10.1172/jci.insight.131597.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAdvanced fibrosisAlveolar surface densityFibrosis progressionLung fibrosisHuman lungDynamic Regulatory Events MinerExtent of fibrosisIPF lungsPulmonary fibrosisControl lungsIPF tissueB lymphocytesFibrosisLungLinear mixed-effects modelsMixed-effects modelsGene expression changesSystems biology modelsDifferential gene expression analysisGene expression analysisProgressionGene expression networksRNA sequencingBiology models
2008
Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis
Lin L, Zhou Z, Zheng L, Alber S, Watkins S, Ray P, Kaminski N, Zhang Y, Morse D. Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis. American Journal Of Pathology 2008, 173: 337-346. PMID: 18583319, PMCID: PMC2475772, DOI: 10.2353/ajpath.2008.070915.Peer-Reviewed Original ResearchConceptsLung fibrosisPulmonary fibrosisGrowth factorSuppression of fibrosisTranscriptional regulator inhibitorIdiopathic pulmonary fibrosisProgressive lung fibrosisEffects of Id1Activation of TGFInhibited DNA bindingProfibrotic functionsDisease progressionFibrosisFibrotic diseasesDifferentiation 1TGFPotential mechanismsId1FibroblastsNovel binding partnerHuman fibroblastsDRIL1Target genesPatientsLung
2001
Interleukin-13 Induces Dramatically Different Transcriptional Programs in Three Human Airway Cell Types
Lee J, Kaminski N, Dolganov G, Grunig G, Koth L, Solomon C, Erle D, Sheppard D. Interleukin-13 Induces Dramatically Different Transcriptional Programs in Three Human Airway Cell Types. American Journal Of Respiratory Cell And Molecular Biology 2001, 25: 474-485. PMID: 11694453, DOI: 10.1165/ajrcmb.25.4.4522.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedEndopeptidasesExtracellular Matrix ProteinsFibroblastsGene Expression RegulationHumansInterleukin-13Ion ChannelsMuscle, SmoothOligonucleotide Array Sequence AnalysisProtease InhibitorsRespiratory MucosaRespiratory SystemSignal TransductionSTAT6 Transcription FactorTrans-ActivatorsTranscription, GeneticConceptsAirway cell typesIL-13Airway epithelial cellsAirway cellsAirway smooth muscle cellsPhenotypic featuresInterleukin-13 inducesResident airway cellsEpithelial cellsImmediate hypersensitivity responsesAirway smooth muscleDevelopment of asthmaCell typesSmooth muscle cellsHypersensitivity responseT lymphocytesSmooth muscleAsthmaB lymphocytesLung fibroblastsMuscle cellsVivo responseCentral mediatorGene expressionPrimary cultures