2019
Gene set meta-analysis with Quantitative Set Analysis for Gene Expression (QuSAGE)
Meng H, Yaari G, Bolen CR, Avey S, Kleinstein SH. Gene set meta-analysis with Quantitative Set Analysis for Gene Expression (QuSAGE). PLOS Computational Biology 2019, 15: e1006899. PMID: 30939133, PMCID: PMC6461294, DOI: 10.1371/journal.pcbi.1006899.Peer-Reviewed Original ResearchMeSH KeywordsComputational BiologyGene ExpressionGene Expression ProfilingHumansInfluenza, HumanProbabilitySoftwareVaccination
2017
Polycomb Repressive Complex 2-Mediated Chromatin Repression Guides Effector CD8+ T Cell Terminal Differentiation and Loss of Multipotency
Gray SM, Amezquita RA, Guan T, Kleinstein SH, Kaech SM. Polycomb Repressive Complex 2-Mediated Chromatin Repression Guides Effector CD8+ T Cell Terminal Differentiation and Loss of Multipotency. Immunity 2017, 46: 596-608. PMID: 28410989, PMCID: PMC5457165, DOI: 10.1016/j.immuni.2017.03.012.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD8-Positive T-LymphocytesCell DifferentiationChromatinEnhancer of Zeste Homolog 2 ProteinFlow CytometryForkhead Box Protein O1Gene ExpressionHistonesImmunoblottingImmunologic MemoryLysineMethylationMice, Inbred C57BLMice, KnockoutMice, TransgenicModels, ImmunologicalMultipotent Stem CellsPolycomb Repressive Complex 2Reverse Transcriptase Polymerase Chain ReactionConceptsH3K27me3 depositionPolycomb repressive complex 2T cell terminal differentiationRepressive complex 2MP cellsLoss of multipotencyPro-survival genesCell terminal differentiationFate restrictionPermissive chromatinEpigenetic silencingMemory cell potentialDevelopmental plasticityCell developmentTerminal differentiationCell differentiationGenesPrecursor cellsFOXO1 expressionChromatinMemory precursor cellsMultipotencyCell maturationClonal expansionCells
2012
Impaired Toll-Like Receptor 3-Mediated Immune Responses from Macrophages of Patients Chronically Infected with Hepatitis C Virus
Qian F, Bolen CR, Jing C, Wang X, Zheng W, Zhao H, Fikrig E, Bruce RD, Kleinstein SH, Montgomery RR. Impaired Toll-Like Receptor 3-Mediated Immune Responses from Macrophages of Patients Chronically Infected with Hepatitis C Virus. MSphere 2012, 20: 146-155. PMID: 23220997, PMCID: PMC3571267, DOI: 10.1128/cvi.00530-12.Peer-Reviewed Original ResearchMeSH KeywordsAdultFemaleGene ExpressionGenotypeHepacivirusHepatitis C, ChronicHumansInflammationInterferon-betaInterferonsInterleukinsLeukocytes, MononuclearMacrophagesMalePhosphorylationPolymorphism, Single NucleotideSignal TransductionSTAT1 Transcription FactorToll-Like Receptor 3Tumor Necrosis Factor-alphaViral LoadConceptsToll-like receptor 3Peripheral blood mononuclear cellsHepatitis C virusImmune responseHCV patientsC virusExpression of TLR3Clearance of HCVCommon chronic blood-borne infectionElevated innate immune responseImpaired toll-like receptorPrimary macrophagesHCV genotype 1Ongoing inflammatory responseMajority of patientsBlood-borne infectionsBlood mononuclear cellsToll-like receptorsIFN response genesPotential therapeutic approachInnate immune responseMacrophages of patientsElevated baseline expressionTLR3 pathwayViral clearance
2011
Altered Folate Availability Modifies the Molecular Environment of the Human Colorectum: Implications for Colorectal Carcinogenesis
Protiva P, Mason JB, Liu Z, Hopkins ME, Nelson C, Marshall JR, Lambrecht RW, Pendyala S, Kopelovich L, Kim M, Kleinstein SH, Laird PW, Lipkin M, Holt PR. Altered Folate Availability Modifies the Molecular Environment of the Human Colorectum: Implications for Colorectal Carcinogenesis. Cancer Prevention Research 2011, 4: 530-543. PMID: 21321062, PMCID: PMC3742550, DOI: 10.1158/1940-6207.capr-10-0143.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBiological AvailabilityCell Transformation, NeoplasticColonColorectal NeoplasmsDietary SupplementsDNA BreaksDNA MethylationFemaleFolic AcidFolic Acid DeficiencyGene ExpressionGene Expression ProfilingHumansMaleMiddle AgedOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticRectumReverse Transcriptase Polymerase Chain ReactionTumor Suppressor Protein p53ConceptsFolate supplementationFolate deliveryFolate depletionImmune responseColorectal carcinogenesisDNA strand breaksHuman colonColorectal cancer riskFolic acidSupplemental folic acidLow-folate dietLow folate statusImmune response pathwaysImmune-related pathwaysFirst studyRectosigmoid biopsiesRisk volunteersPrimary endpointGene array analysisPromoter-specific DNA methylationRepletion protocolFolate dietFolate levelsSecond studyFolate status
2009
Salmonella Typhimurium Type III Secretion Effectors Stimulate Innate Immune Responses in Cultured Epithelial Cells
Bruno VM, Hannemann S, Lara-Tejero M, Flavell RA, Kleinstein SH, Galán JE. Salmonella Typhimurium Type III Secretion Effectors Stimulate Innate Immune Responses in Cultured Epithelial Cells. PLOS Pathogens 2009, 5: e1000538. PMID: 19662166, PMCID: PMC2714975, DOI: 10.1371/journal.ppat.1000538.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBacterial ProteinsBlotting, WesternCell LineColitisEpithelial CellsGene ExpressionGene Expression ProfilingGuanine Nucleotide Exchange FactorsHumansImmunity, InnateMiceMitogen-Activated Protein Kinase KinasesMyotonin-Protein KinaseNF-kappa BOligonucleotide Array Sequence AnalysisProtein Serine-Threonine KinasesReverse Transcriptase Polymerase Chain ReactionSalmonella InfectionsSalmonella typhimuriumSignal TransductionTranscription, GeneticConceptsInnate immune receptorsInnate immune responseIntestinal inflammationImmune responseEpithelial cellsBacterial productsIntestinal inflammatory pathologyImmune receptorsCultured epithelial cellsEnteric pathogen Salmonella typhimuriumInnate immune systemIntestinal epithelial cellsInflammatory pathologyInflammatory responseType III secretion effectorsImmune systemSalmonella typhimuriumNF-kappaBMitogen-activated protein kinaseEnteric pathogensPathogen Salmonella typhimuriumPathologyReceptorsInflammationType III secretion system