2019
BAL Cell Gene Expression Is Indicative of Outcome and Airway Basal Cell Involvement in Idiopathic Pulmonary Fibrosis
Prasse A, Binder H, Schupp JC, Kayser G, Bargagli E, Jaeger B, Hess M, Rittinghausen S, Vuga L, Lynn H, Violette S, Jung B, Quast K, Vanaudenaerde B, Xu Y, Hohlfeld JM, Krug N, Herazo-Maya JD, Rottoli P, Wuyts WA, Kaminski N. BAL Cell Gene Expression Is Indicative of Outcome and Airway Basal Cell Involvement in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2019, 199: 622-630. PMID: 30141961, PMCID: PMC6396865, DOI: 10.1164/rccm.201712-2551oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAirway basal cellsChronic obstructive pulmonary diseaseObstructive pulmonary diseasePulmonary diseaseBAL cellsBasal cellsPulmonary fibrosisControl subjectsCell gene expressionIndependent IPF cohortsNine-gene signatureIPF cohortDerivation cohortClinical parametersRetrospective studyUnivariate analysisUnpredictable courseCell involvementDiscovery cohortGene expressionHealthy volunteersCox modelStage IIIFatal disease
2017
Validation of a 52-gene risk profile for outcome prediction in patients with idiopathic pulmonary fibrosis: an international, multicentre, cohort study
Herazo-Maya JD, Sun J, Molyneaux PL, Li Q, Villalba JA, Tzouvelekis A, Lynn H, Juan-Guardela BM, Risquez C, Osorio JC, Yan X, Michel G, Aurelien N, Lindell KO, Klesen MJ, Moffatt MF, Cookson WO, Zhang Y, Garcia JGN, Noth I, Prasse A, Bar-Joseph Z, Gibson KF, Zhao H, Herzog EL, Rosas IO, Maher TM, Kaminski N. Validation of a 52-gene risk profile for outcome prediction in patients with idiopathic pulmonary fibrosis: an international, multicentre, cohort study. The Lancet Respiratory Medicine 2017, 5: 857-868. PMID: 28942086, PMCID: PMC5677538, DOI: 10.1016/s2213-2600(17)30349-1.Peer-Reviewed Original ResearchMeSH KeywordsAgedCohort StudiesFemaleGene Expression ProfilingGenetic MarkersGenetic TestingHumansIdiopathic Pulmonary FibrosisLeukocytes, MononuclearLinear ModelsMaleMiddle AgedOligonucleotide Array Sequence AnalysisPrognosisProportional Hazards ModelsRisk AssessmentRisk FactorsTime FactorsVital CapacityConceptsIdiopathic pulmonary fibrosisTransplant-free survivalRisk profilePulmonary fibrosisAntifibrotic drugsPeripheral blood mononuclear cellsCox proportional hazards modelClinical prediction toolGroup of patientsBlood mononuclear cellsHigh-risk groupProportional hazards modelPulmonary Fibrosis FoundationPittsburgh cohortUntreated patientsCohort studyClinical courseIPF diagnosisBlood InstituteProspective studyVital capacityMononuclear cellsPeripheral bloodUS National InstitutesNational Heart
2016
Integrated Genomics Reveals Convergent Transcriptomic Networks Underlying Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis
Kusko RL, Brothers JF, Tedrow J, Pandit K, Huleihel L, Perdomo C, Liu G, Juan-Guardela B, Kass D, Zhang S, Lenburg M, Martinez F, Quackenbush J, Sciurba F, Limper A, Geraci M, Yang I, Schwartz DA, Beane J, Spira A, Kaminski N. Integrated Genomics Reveals Convergent Transcriptomic Networks Underlying Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2016, 194: 948-960. PMID: 27104832, PMCID: PMC5067817, DOI: 10.1164/rccm.201510-2026oc.Peer-Reviewed Original ResearchMeSH KeywordsAdultEmphysemaFemaleGene Regulatory NetworksHumansHypoxia-Inducible Factor 1, alpha SubunitIdiopathic Pulmonary FibrosisI-kappa B ProteinsMaleMembrane ProteinsMiddle AgedNerve Tissue ProteinsOligonucleotide Array Sequence AnalysisPlatelet-Derived Growth FactorProto-Oncogene Proteins c-mdm2Pulmonary Disease, Chronic ObstructiveConceptsChronic obstructive pulmonary diseaseIdiopathic pulmonary fibrosisObstructive pulmonary diseasePulmonary diseasePulmonary fibrosisNCounter Analysis SystemHypoxia pathwayQuantitative polymerase chain reactionTranscriptomic pathwaysPolymerase chain reactionIndependent cohortEmphysemaIndependent sample setDiseaseGene expression arraysEnvironmental exposuresChain reactionFibrosisLungMolecular mechanismsExpression arraysMiR96Integrative genomics approachTranscriptional regulatory hubsPathway
2015
A functional genomic model for predicting prognosis in idiopathic pulmonary fibrosis
Huang Y, Ma SF, Vij R, Oldham JM, Herazo-Maya J, Broderick SM, Strek ME, White SR, Hogarth DK, Sandbo NK, Lussier YA, Gibson KF, Kaminski N, Garcia JG, Noth I. A functional genomic model for predicting prognosis in idiopathic pulmonary fibrosis. BMC Pulmonary Medicine 2015, 15: 147. PMID: 26589497, PMCID: PMC4654815, DOI: 10.1186/s12890-015-0142-8.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPrognostic indexIPF patientsPulmonary fibrosisValidation cohortTraining cohortMultivariate Cox regression survival analysisPrognostic modelPeripheral blood mononuclear cellsUnivariate Cox regression analysisCox regression survival analysisLow-risk patientsWeighted gene co-expression network analysisCox regression analysisBlood mononuclear cellsCourse of diseaseIndependent validation cohortRegression survival analysisNovel prognostic modelPredictor genesT cell biologyT cell receptorCurrent prognostic toolsFunctional pathway analysisFold change
2014
Gene Expression in Relation to Exhaled Nitric Oxide Identifies Novel Asthma Phenotypes with Unique Biomolecular Pathways
Modena BD, Tedrow JR, Milosevic J, Bleecker ER, Meyers DA, Wu W, Bar-Joseph Z, Erzurum SC, Gaston BM, Busse WW, Jarjour NN, Kaminski N, Wenzel SE. Gene Expression in Relation to Exhaled Nitric Oxide Identifies Novel Asthma Phenotypes with Unique Biomolecular Pathways. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 1363-1372. PMID: 25338189, PMCID: PMC4294630, DOI: 10.1164/rccm.201406-1099oc.Peer-Reviewed Original ResearchMeSH KeywordsAdultAsthmaBiomarkersBronchiCase-Control StudiesFemaleGene ExpressionHumansMaleMiddle AgedMultigene FamilyNitric OxideOligonucleotide Array Sequence AnalysisPhenotypeReal-Time Polymerase Chain ReactionConceptsEpithelial cell gene expressionCell gene expressionGene expressionAirway epithelial cell gene expressionGene expression patternsSevere Asthma Research ProgramActin cytoskeletonGene clusterGenomic studiesGene transcriptionGene pathwaysMolecular basisExpression patternsAsthma phenotypesWnt pathwayMicroarray platformGenesNovel pathwayPhenotypeBiomolecular pathwaysNeuronal functionPathwayUnadjusted p-valuesExpressionBiological characteristicsSecreted Phosphoprotein 1 Is a Determinant of Lung Function Development in Mice
Ganguly K, Martin TM, Concel VJ, Upadhyay S, Bein K, Brant KA, George L, Mitra A, Thimraj TA, Fabisiak JP, Vuga LJ, Fattman C, Kaminski N, Schulz H, Leikauf GD. Secreted Phosphoprotein 1 Is a Determinant of Lung Function Development in Mice. American Journal Of Respiratory Cell And Molecular Biology 2014, 51: 637-651. PMID: 24816281, PMCID: PMC4224082, DOI: 10.1165/rcmb.2013-0471oc.Peer-Reviewed Original ResearchMeSH KeywordsAlveolar Epithelial CellsAnimalsAnimals, NewbornCore Binding Factor Alpha 1 SubunitFemaleGene Expression Regulation, DevelopmentalLung ComplianceMaleMice, Inbred C3HMice, Inbred C57BLMice, KnockoutOligonucleotide Array Sequence AnalysisOsteopontinPromoter Regions, GeneticPulmonary AlveoliPulmonary Disease, Chronic ObstructiveReceptor, Notch1ConceptsMicroarray analysisPhosphoprotein 1Quantitative trait lociLung functionQuantitative RT-PCR analysisDNA-protein bindingRunt-related transcription factor 2Transcription factor 2Developmental transcriptsLung developmentTrait lociNumerous genesSecreted Phosphoprotein 1Notch1 transcriptsRT-PCR analysisInsulin-like growth factor-1C3H/HeJ miceDiminished lung functionLung function developmentSPP1 promoterSPP1Growth factor-1Mean airspace chord lengthC3H/HeJGenetic variantsC-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis
Vuga LJ, Tedrow JR, Pandit KV, Tan J, Kass DJ, Xue J, Chandra D, Leader JK, Gibson KF, Kaminski N, Sciurba FC, Duncan SR. C-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 966-974. PMID: 24628285, PMCID: PMC4098096, DOI: 10.1164/rccm.201309-1592oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overBiomarkersCase-Control StudiesChemokine CXCL13Disease ProgressionEnzyme-Linked Immunosorbent AssayFemaleHumansIdiopathic Pulmonary FibrosisImmunohistochemistryMaleMiddle AgedOligonucleotide Array Sequence AnalysisPredictive Value of TestsPrognosisPulmonary Disease, Chronic ObstructiveRisk FactorsSensitivity and SpecificitySeverity of Illness IndexConceptsChronic obstructive pulmonary diseaseC motif chemokine 13IPF lungsPrognostic biomarkerB cellsIdiopathic pulmonary fibrosis (IPF) pathogenesisB cell-targeted therapiesAntibody-mediated syndromeDysregulated B cellsPulmonary fibrosis pathogenesisPulmonary artery hypertensionObstructive pulmonary diseaseIdiopathic pulmonary fibrosisSix-month survivalB-cell traffickingAcute exacerbationArtery hypertensionCXCL13 mRNAPlasma CXCL13IPF pathogenesisRespiratory failureLung injuryCXCL13 concentrationsPulmonary diseaseRadiographic emphysemaAging Mesenchymal Stem Cells Fail to Protect Because of Impaired Migration and Antiinflammatory Response
Bustos ML, Huleihel L, Kapetanaki MG, Lino-Cardenas CL, Mroz L, Ellis BM, McVerry BJ, Richards TJ, Kaminski N, Cerdenes N, Mora AL, Rojas M. Aging Mesenchymal Stem Cells Fail to Protect Because of Impaired Migration and Antiinflammatory Response. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 787-798. PMID: 24559482, PMCID: PMC4061541, DOI: 10.1164/rccm.201306-1043oc.Peer-Reviewed Original ResearchConceptsBone marrow-derived MSCsMesenchymal stem cellsChemokine receptorsAcute lung injuryAcute lung diseaseSite of injuryAge-dependent decreaseBone marrow-derived mesenchymal stem cellsMarrow-derived mesenchymal stem cellsInflammatory response genesSuch age-related changesAge-related phenomenonStem cellsAge-related changesAdoptive transferLung injuryEndotoxemic miceLung diseaseAntiinflammatory responseFunctional impairmentMore inflammationProtective effectOld miceParacrine mechanismsAlveolar epithelium
2013
Peripheral Blood Mononuclear Cell Gene Expression Profiles Predict Poor Outcome in Idiopathic Pulmonary Fibrosis
Herazo-Maya JD, Noth I, Duncan SR, Kim S, Ma SF, Tseng GC, Feingold E, Juan-Guardela BM, Richards TJ, Lussier Y, Huang Y, Vij R, Lindell KO, Xue J, Gibson KF, Shapiro SD, Garcia JG, Kaminski N. Peripheral Blood Mononuclear Cell Gene Expression Profiles Predict Poor Outcome in Idiopathic Pulmonary Fibrosis. Science Translational Medicine 2013, 5: 205ra136. PMID: 24089408, PMCID: PMC4175518, DOI: 10.1126/scitranslmed.3005964.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkersCD28 AntigensCD4 AntigensCluster AnalysisCohort StudiesGene Expression ProfilingHumansIdiopathic Pulmonary FibrosisLeukocytes, MononuclearOligonucleotide Array Sequence AnalysisReproducibility of ResultsReverse Transcriptase Polymerase Chain ReactionSignal TransductionTreatment OutcomeConceptsTransplant-free survivalIdiopathic pulmonary fibrosisPeripheral blood mononuclear cell gene expression profilesReplication cohortCell gene expression profilesPoor outcomePulmonary fibrosisQuantitative reverse transcription polymerase chain reactionReverse transcription-polymerase chain reactionProportional hazards modelTranscription-polymerase chain reactionGene expression profilesPotential cellular sourcesT cell activationIPF patientsLung transplantationMicroarray cohortPatient ageOutcome biomarkerPatient groupVital capacityPolymerase chain reactionT cellsDiscovery cohortITK expressionFunctional Genomic Assessment of Phosgene-Induced Acute Lung Injury in Mice
Leikauf GD, Concel VJ, Bein K, Liu P, Berndt A, Martin TM, Ganguly K, Jang AS, Brant KA, Dopico RA, Upadhyay S, Cario C, Di YP, Vuga LJ, Kostem E, Eskin E, You M, Kaminski N, Prows DR, Knoell DL, Fabisiak JP. Functional Genomic Assessment of Phosgene-Induced Acute Lung Injury in Mice. American Journal Of Respiratory Cell And Molecular Biology 2013, 49: 130522202035005. PMID: 23590305, PMCID: PMC3824050, DOI: 10.1165/rcmb.2012-0337oc.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAllelesAnimalsChemical Warfare AgentsChromosome MappingElectrophoretic Mobility Shift AssayFemaleGene ExpressionGene Expression ProfilingGenomeGenome-Wide Association StudyGenomicsGenotypeIntegrinsLungMiceMice, Inbred StrainsOligonucleotide Array Sequence AnalysisPhosgenePolymorphism, Single NucleotidePromoter Regions, GeneticReelin ProteinSodium-Potassium-Exchanging ATPaseConceptsSignificant SNP associationsSNP associationsTranscriptomic analysisCompetitive electrophoretic mobility shift analysisGenome-wide association mappingFunctional genomic assessmentPutative transcription factorElectrophoretic mobility shift analysisMobility shift analysisAssociation mappingGenetic resolutionTranscription factorsCandidate genesFunctional domainsNonsynonymous SNPsGenomic assessmentPhenotypic differencesPhenotypic extremesDiverse panelGenesGenetic determinantsShift analysisPTPRTAllelesITGA9Expression of Regulatory Platelet MicroRNAs in Patients with Sickle Cell Disease
Jain S, Kapetanaki MG, Raghavachari N, Woodhouse K, Yu G, Barge S, Coronnello C, Benos PV, Kato GJ, Kaminski N, Gladwin MT. Expression of Regulatory Platelet MicroRNAs in Patients with Sickle Cell Disease. PLOS ONE 2013, 8: e60932. PMID: 23593351, PMCID: PMC3625199, DOI: 10.1371/journal.pone.0060932.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnemia, Sickle CellBlood PlateletsCell LineChromosomes, Human, Pair 14Computational BiologyDown-RegulationFemaleGene Expression ProfilingGene Expression RegulationGenomic ImprintingHumansHydroxyureaMaleMegakaryocytesMicroRNAsMiddle AgedMolecular Sequence AnnotationOligonucleotide Array Sequence AnalysisReproducibility of ResultsTricuspid Valve InsufficiencyUp-RegulationYoung AdultConceptsMiRNA expression profilesExpression profilesMRNA targetsSignificant transcriptional repressionPlatelet miRNAsPost-transcriptional regulationMiRNA target sequencesComputational prediction analysisAltered miRNA expression profilesMRNA expression profilesExpression of miRNAsAgilent miRNA microarrayTranscriptional repressionPlatelet transcriptomeBiological pathwaysDownregulated miRNAsMiRNAsPlatelet transcriptsMiRNA microarrayPlatelet microRNAsTarget sequenceMiR-376aMiR-376QRT-PCRMiR-154
2012
Profibrotic Role of miR-154 in Pulmonary Fibrosis
Milosevic J, Pandit K, Magister M, Rabinovich E, Ellwanger DC, Yu G, Vuga LJ, Weksler B, Benos PV, Gibson KF, McMillan M, Kahn M, Kaminski N. Profibrotic Role of miR-154 in Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2012, 47: 879-887. PMID: 23043088, PMCID: PMC3547095, DOI: 10.1165/rcmb.2011-0377oc.Peer-Reviewed Original ResearchMeSH KeywordsCase-Control StudiesCell MovementCell ProliferationCells, CulturedChromosomes, Human, Pair 14Cyclin-Dependent Kinase Inhibitor p15FibroblastsGene ExpressionHumansLungMicroRNAsMultigene FamilyOligonucleotide Array Sequence AnalysisPulmonary FibrosisRNA InterferenceTranscriptomeTransforming Growth Factor beta1Wnt Signaling PathwayConceptsIdiopathic pulmonary fibrosisNormal human lung fibroblastsMiR-154IPF lungsPulmonary fibrosisIPF fibroblastsProgressive interstitial lung diseaseInterstitial lung diseaseWnt/β-catenin pathwayHuman lung fibroblastsΒ-catenin pathwayTGF-β1 stimulationBinding of Smad3Quantitative RT-PCRLung diseaseProfibrotic roleExpression of microRNAsICG-001MiR-134Unknown originMiR-382MiR-487bProliferative effectLung fibroblastsMiR-410Matrix Metalloproteinase-19 Is a Key Regulator of Lung Fibrosis in Mice and Humans
Yu G, Kovkarova-Naumovski E, Jara P, Parwani A, Kass D, Ruiz V, Lopez-Otín C, Rosas IO, Gibson KF, Cabrera S, Ramírez R, Yousem SA, Richards TJ, Chensny LJ, Selman M, Kaminski N, Pardo A. Matrix Metalloproteinase-19 Is a Key Regulator of Lung Fibrosis in Mice and Humans. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 752-762. PMID: 22859522, PMCID: PMC5450991, DOI: 10.1164/rccm.201202-0302oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinCells, CulturedCyclooxygenase 2Epithelial CellsGene Expression Regulation, EnzymologicHumansIdiopathic Pulmonary FibrosisLaser Capture MicrodissectionMatrix Metalloproteinases, SecretedMiceMice, KnockoutOligonucleotide Array Sequence AnalysisPulmonary AlveoliUp-RegulationConceptsIdiopathic pulmonary fibrosisHyperplastic epithelial cellsAlveolar epithelial cellsEpithelial cellsMMP-19IPF lungsWT miceLung fibrosisFibrotic responseHyperplastic alveolar epithelial cellsNovel mediatorLaser capture microscopeLung fibrotic responseDevelopment of fibrosisWild-type miceEpithelial phenotypic changesMatrix metalloproteinase-19Microarray analysisA549 epithelial cellsLung injuryBronchoalveolar lavagePulmonary fibrosisLung tissueSame lungFibrosisRetinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema
Shi Y, Cao J, Gao J, Zheng L, Goodwin A, An CH, Patel A, Lee JS, Duncan SR, Kaminski N, Pandit KV, Rosas IO, Choi AM, Morse D. Retinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 412-419. PMID: 22744720, PMCID: PMC5450975, DOI: 10.1164/rccm.201111-2023oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersCells, CulturedDisease Models, AnimalDNA DamageDNA RepairGene Expression ProfilingHumansLungMiceMice, Inbred C57BLMice, Neurologic MutantsNuclear Receptor Subfamily 1, Group F, Member 1Oligonucleotide Array Sequence AnalysisPulmonary Disease, Chronic ObstructivePulmonary EmphysemaTobacco Smoke PollutionConceptsRetinoic acid-related orphan receptorAcid-related orphan receptorCigarette smoke extractLungs of patientsPathogenesis of emphysemaRORA expressionCigarette smokeAirspace enlargementSmoke extractCigarette smoke exposureSmoke-induced emphysemaOrphan receptorDNA damageActive smokingLung transplantationSmoke exposureLung cancerPulmonary emphysemaLung tissueEmphysemaPatientsGene expression profilingApoptotic cell deathMiceEnhanced susceptibility
2011
MetaQC: objective quality control and inclusion/exclusion criteria for genomic meta-analysis
Kang DD, Sibille E, Kaminski N, Tseng GC. MetaQC: objective quality control and inclusion/exclusion criteria for genomic meta-analysis. Nucleic Acids Research 2011, 40: e15-e15. PMID: 22116060, PMCID: PMC3258120, DOI: 10.1093/nar/gkr1071.Peer-Reviewed Original ResearchMouse Conjunctival Forniceal Gene Expression during Postnatal Development and Its Regulation by Krüppel-like Factor 4
Gupta D, Harvey SA, Kaminski N, Swamynathan SK. Mouse Conjunctival Forniceal Gene Expression during Postnatal Development and Its Regulation by Krüppel-like Factor 4. Investigative Ophthalmology & Visual Science 2011, 52: 4951-4962. PMID: 21398290, PMCID: PMC3176043, DOI: 10.1167/iovs.10-7068.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsConjunctivaEpithelial CellsFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalGenotypeGoblet CellsIn Situ HybridizationKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMiceOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionTranscription FactorsConceptsKLF4 target genesGene expressionTarget genesEts transcription factor family memberCell developmentTranscription factor family membersGene regulatory networksGoblet cell developmentLaser microdissectionComponents of pathwaysTranscription factor SPDEFFactor family membersMesenchymal-epithelial transitionKrüppel-like factor 4Regulatory networksRegulatory targetsRole of KLF4Spatiotemporal expressionQuantitative RT-PCRGlycoprotein biosynthesisMucosal epitheliumGoblet cellsGenesKLF4TranscriptsHigh Throughput Determination of TGFβ1/SMAD3 Targets in A549 Lung Epithelial Cells
Zhang Y, Handley D, Kaplan T, Yu H, Bais AS, Richards T, Pandit KV, Zeng Q, Benos PV, Friedman N, Eickelberg O, Kaminski N. High Throughput Determination of TGFβ1/SMAD3 Targets in A549 Lung Epithelial Cells. PLOS ONE 2011, 6: e20319. PMID: 21625455, PMCID: PMC3098871, DOI: 10.1371/journal.pone.0020319.Peer-Reviewed Original ResearchMeSH KeywordsBase SequenceCell LineChromatin ImmunoprecipitationDNA PrimersElectrophoretic Mobility Shift AssayEpithelial CellsHumansLungOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticProtein BindingReverse Transcriptase Polymerase Chain ReactionSmad3 ProteinTransforming Growth Factor beta1ConceptsGene expression microarraysLung epithelial cellsMolecular pathwaysTranscriptional regulationExpression microarraysGlobal transcriptional regulationTGFβ1/Smad3Epithelial cellsHuman promoter regionsSignal transduction cascadeTarget gene expressionEpithelial cell phenotypeGene expression analysisTranscription factor Smad3Primary lung epithelial cellsSmad3 targetsQuantitative real-time RT-PCRFOXA2 promoterHuman A549 alveolar epithelial cellsChromatin immunoprecipitationTransduction cascadeTarget genesA549 lung epithelial cellsExpression analysisGene expression
2010
Module-based prediction approach for robust inter-study predictions in microarray data
Mi Z, Shen K, Song N, Cheng C, Song C, Kaminski N, Tseng GC. Module-based prediction approach for robust inter-study predictions in microarray data. Bioinformatics 2010, 26: 2586-2593. PMID: 20719761, PMCID: PMC2951088, DOI: 10.1093/bioinformatics/btq472.Peer-Reviewed Original ResearchCluster AnalysisComputational BiologyDatabases, FactualGene Expression ProfilingOligonucleotide Array Sequence Analysis
2009
Chronic lung diseases
Wu W, Kaminski N. Chronic lung diseases. WIREs Mechanisms Of Disease 2009, 1: 298-308. PMID: 20835999, DOI: 10.1002/wsbm.23.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChronic DiseaseGene Expression ProfilingGenome-Wide Association StudyHigh-Throughput Screening AssaysHumansLung DiseasesMicroRNAsModels, BiologicalOligonucleotide Array Sequence AnalysisProteomicsSystems BiologyConceptsSystems biology approachBiology approachChronic lung diseaseComplex human diseasesHigh-throughput technologiesLung diseaseSystems biologyHuman diseasesTraditional experimental approachesComplex lung diseaseBiomedical researchExperimental approachSerious economic burdenHigh morbiditySerious threatHuman healthEconomic burdenMortality rateDiseaseBiologyMicroarrayPromising findingsFACS-Assisted Microarray Profiling Implicates Novel Genes and Pathways in Zebrafish Gastrointestinal Tract Development
Stuckenholz C, Lu L, Thakur P, Kaminski N, Bahary N. FACS-Assisted Microarray Profiling Implicates Novel Genes and Pathways in Zebrafish Gastrointestinal Tract Development. Gastroenterology 2009, 137: 1321-1332. PMID: 19563808, PMCID: PMC2785077, DOI: 10.1053/j.gastro.2009.06.050.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedCell SeparationChromosomes, Human, Pair 8Digestive System NeoplasmsFlow CytometryGastrointestinal TractGene Expression ProfilingGene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticGene Regulatory NetworksGreen Fluorescent ProteinsHumansIn Situ HybridizationLarvaMicroRNAsOligonucleotide Array Sequence AnalysisOrganogenesisReproducibility of ResultsTime FactorsZebrafishZebrafish ProteinsConceptsFluorescence-activated cell sortingNovel genesGreen fluorescent proteinGene networksPutative transcription factorTransgenic zebrafish lineZebrafish Danio rerioPhosphatidylinositol-3-kinase (PI3K) pathwayExcellent model systemDevelopmental time pointsChromosome arm 8qGastrointestinal developmentZebrafish lineHuman orthologDanio rerioTranscription factorsKinase pathwayMicroarray profilingFluorescent proteinGFP expressionGenesNovel pathwayGFP cellsCell sortingOrganogenesis