2018
Surfactant protein C dampens inflammation by decreasing JAK/STAT activation during lung repair
Jin H, Ciechanowicz AK, Kaplan AR, Wang L, Zhang P, Lu YC, Tobin RE, Tobin BA, Cohn L, Zeiss CJ, Lee PJ, Bruscia EM, Krause DS. Surfactant protein C dampens inflammation by decreasing JAK/STAT activation during lung repair. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2018, 314: l882-l892. PMID: 29345196, PMCID: PMC6008135, DOI: 10.1152/ajplung.00418.2017.Peer-Reviewed Original ResearchConceptsAcute respiratory distress syndromeKO miceSurfactant protein CClinical acute respiratory distress syndromeProtein CAlveolar type 2 cellsAnti-inflammatory mediatorsRespiratory distress syndromeBronchoalveolar lavage fluidAnti-inflammatory moleculesPhosphorylated signal transductionType 2 cellsSPC expressionInducible suicide geneJanus kinaseLevels of suppressorDistress syndromeBAL fluidGranulocyte infiltrationJAK1/2 inhibitorLavage fluidProinflammatory phenotypeInflammatory cytokinesSevere inflammationInjury model
2017
Ezrin links CFTR to TLR4 signaling to orchestrate anti-bacterial immune response in macrophages
Di Pietro C, Zhang PX, O’Rourke T, Murray TS, Wang L, Britto CJ, Koff JL, Krause DS, Egan ME, Bruscia EM. Ezrin links CFTR to TLR4 signaling to orchestrate anti-bacterial immune response in macrophages. Scientific Reports 2017, 7: 10882. PMID: 28883468, PMCID: PMC5589856, DOI: 10.1038/s41598-017-11012-7.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell LineCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorCytoskeletal ProteinsDisease Models, AnimalMacrophage ActivationMacrophagesMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPseudomonas aeruginosaPseudomonas InfectionsSignal TransductionToll-Like Receptor 4ConceptsCystic fibrosis transmembrane conductance regulatorPI3K/AktFibrosis transmembrane conductance regulatorTransmembrane conductance regulatorPI3K/Akt signalingConductance regulatorAnti-bacterial immune responseAkt signalingAltered localizationEzrinCystic fibrosis diseaseMφ activationAktProtein levelsFibrosis diseaseActivationImmune regulationPhagocytosisInductionDirect linkSignalingRegulatorImmune responseMΦMacrophages
2012
Induction of megakaryocyte differentiation drives nuclear accumulation and transcriptional function of MKL1 via actin polymerization and RhoA activation
Smith EC, Teixeira AM, Chen RC, Wang L, Gao Y, Hahn KL, Krause DS. Induction of megakaryocyte differentiation drives nuclear accumulation and transcriptional function of MKL1 via actin polymerization and RhoA activation. Blood 2012, 121: 1094-1101. PMID: 23243284, PMCID: PMC3575755, DOI: 10.1182/blood-2012-05-429993.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCell DifferentiationCell Line, TumorCell NucleusDNA-Binding ProteinsEnzyme ActivationHumansMegakaryocyte Progenitor CellsMegakaryocytesMiceOncogene Proteins, FusionProtein MultimerizationRhoA GTP-Binding ProteinSerum Response FactorTetradecanoylphorbol AcetateThrombopoietinTrans-ActivatorsConceptsMegakaryocyte differentiationActin polymerizationSubcellular localizationSerum response factor (SRF) transcriptional activityRhoA activitySRF target genesComplex cellular responsesFactor transcriptional activityMuscle cell typesCell-type specificHuman erythroleukemia cellsPrimary megakaryocytesTranscriptional regulatorsActin organizationCellular functionsTranscriptional functionSRF activityNuclear localizationTarget genesMegakaryocytic differentiationTranscriptional activityNuclear accumulationErythroleukemia cellsMolecular mechanismsRhoA activationRole of RhoA-Specific Guanine Exchange Factors in Regulation of Endomitosis in Megakaryocytes
Gao Y, Smith E, Ker E, Campbell P, Cheng EC, Zou S, Lin S, Wang L, Halene S, Krause DS. Role of RhoA-Specific Guanine Exchange Factors in Regulation of Endomitosis in Megakaryocytes. Developmental Cell 2012, 22: 573-584. PMID: 22387001, PMCID: PMC3306542, DOI: 10.1016/j.devcel.2011.12.019.Peer-Reviewed Original ResearchConceptsGEF-H1Efficient platelet productionExchange factor GEF-H1Guanine exchange factorGEF-H1 knockdownDevelopment of aneuploidyGEF-H1 expressionMK polyploidizationExchange factorPloidy defectsAberrant mitosisDevelopmental processesExogenous expressionPolyploidizationRhoA activationEndomitotic cyclePrimary cellsUnknown mechanismMechanistic insightsECT2EndomitosisAneuploid cancersPlatelet productionMegakaryocytesDownregulation
2007
Rbm15 Modulates Notch-Induced Transcriptional Activation and Affects Myeloid Differentiation
Ma X, Renda MJ, Wang L, Cheng EC, Niu C, Morris SW, S. AS, Krause DS. Rbm15 Modulates Notch-Induced Transcriptional Activation and Affects Myeloid Differentiation. Molecular And Cellular Biology 2007, 27: 3056-3064. PMID: 17283045, PMCID: PMC1899951, DOI: 10.1128/mcb.01339-06.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBasic Helix-Loop-Helix Transcription FactorsCell NucleusCHO CellsCricetinaeCricetulusDNA-Binding ProteinsDrosophila ProteinsGene Expression ProfilingHomeodomain ProteinsImmunoglobulin J Recombination Signal Sequence-Binding ProteinMiceMolecular Sequence DataMyeloid CellsMyelopoiesisNuclear ProteinsPromoter Regions, GeneticProtein BindingProtein Structure, TertiaryProtein TransportReceptors, NotchRNA, MessengerRNA, Small InterferingRNA-Binding ProteinsTranscription Factor HES-1Transcription, GeneticTranscriptional ActivationConceptsN-terminusPromoter activityMyeloid differentiationCell linesCell type-specific mannerMyeloid precursor cell linePrimary murine cellsType-specific mannerDominant negative effectStimulation of NotchHematopoietic cell linesHuman erythroleukemia cellsPrecursor cell lineMurine cell linesHematopoietic stem cellsTranscriptional activationHes1 transcriptionRNA interferenceErythroleukemia cellsFusion proteinHes1 promoter activityMurine cellsFusion partnerHematopoietic cellsRBM15