2016
Adenosine-to-inosine RNA editing by ADAR1 is essential for normal murine erythropoiesis
Liddicoat BJ, Hartner JC, Piskol R, Ramaswami G, Chalk AM, Kingsley PD, Sankaran VG, Wall M, Purton LE, Seeburg PH, Palis J, Orkin SH, Lu J, Li JB, Walkley CR. Adenosine-to-inosine RNA editing by ADAR1 is essential for normal murine erythropoiesis. Experimental Hematology 2016, 44: 947-963. PMID: 27373493, PMCID: PMC5035604, DOI: 10.1016/j.exphem.2016.06.250.Peer-Reviewed Original ResearchMeSH KeywordsAdenosineAdenosine DeaminaseAnimalsCluster AnalysisErythrocyte IndicesErythroid CellsErythropoiesisGene ExpressionGene Expression ProfilingGene Expression Regulation, DevelopmentalGene Knockout TechniquesGranulocytesHematopoietic Stem Cell TransplantationInosineInterferonsMiceMicroRNAsMyelopoiesisOrgan SpecificityPhenotypeReceptors, InterferonRetroelementsRNA EditingRNA-Binding ProteinsSignal TransductionTranscription, GeneticConceptsRNA editingErythroid cellsNormal erythropoiesisHematopoietic stem/progenitorsHematopoietic cell typesInnate immune signalingStem/progenitorsEditing eventsErythroid-specific transcriptsEssential functionsImmune signalingMurine erythropoiesisADAR1Cell deathCell typesMyeloid-restricted deletionEditingRNAMicroRNA levelsErythropoiesisCellsProfound activationTranscriptsSignalingAdenosine
2015
Pharmacological modulation of the AKT/microRNA-199a-5p/CAV1 pathway ameliorates cystic fibrosis lung hyper-inflammation
Zhang PX, Cheng J, Zou S, D'Souza AD, Koff JL, Lu J, Lee PJ, Krause DS, Egan ME, Bruscia EM. Pharmacological modulation of the AKT/microRNA-199a-5p/CAV1 pathway ameliorates cystic fibrosis lung hyper-inflammation. Nature Communications 2015, 6: 6221. PMID: 25665524, PMCID: PMC4324503, DOI: 10.1038/ncomms7221.Peer-Reviewed Original ResearchConceptsCF macrophagesMiR-199aMicroRNA-199aHyper-inflammatory responseCFTR-deficient miceCystic fibrosis patientsCystic fibrosis lungLung destructionDisease morbidityPharmacological modulationCF miceCF lungFibrosis patientsInnate immunityLungMacrophagesCAV1 expressionDrug celecoxibReduced levelsTLR4CelecoxibMiceCav1PathwayMorbiditymicroRNA Expression Profiling: Technologies, Insights, and Prospects
Roden C, Mastriano S, Wang N, Lu J. microRNA Expression Profiling: Technologies, Insights, and Prospects. Advances In Experimental Medicine And Biology 2015, 888: 409-421. PMID: 26663195, DOI: 10.1007/978-3-319-22671-2_21.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceCell Line, TumorDisease Models, AnimalGene Expression ProfilingGene Expression Regulation, NeoplasticHigh-Throughput Nucleotide SequencingHumansMicroRNAsMolecular Sequence DataNeoplasmsReverse Transcriptase Polymerase Chain ReactionSequence Homology, Nucleic AcidSignal TransductionConceptsLong small noncoding RNAsExpression profilingMiRNA isoformsMiRNA expressionProfiling technologiesDiverse biological processesSingle-cell variabilitySmall noncoding RNAsMiRNA profiling technologiesGlobal miRNA expressionNext-generation sequencingNoncoding RNAsCell variabilitySingle-molecule measurementsBiological functionsBiological processesTumor suppressorMicroRNA researchQuantitative RT-PCRCareful experimental designMiRNAsIsoformsRT-PCRProfilingExpression
2014
A Functional Screen Identifies miRs That Induce Radioresistance in Glioblastomas
Moskwa P, Zinn PO, Choi YE, Shukla SA, Fendler W, Chen CC, Lu J, Golub TR, Hjelmeland A, Chowdhury D. A Functional Screen Identifies miRs That Induce Radioresistance in Glioblastomas. Molecular Cancer Research 2014, 12: 1767-1778. PMID: 25256711, PMCID: PMC4386891, DOI: 10.1158/1541-7786.mcr-14-0268.Peer-Reviewed Original ResearchConceptsCell cycle checkpoint responsesFunctional screen identifiesTGFβ receptor inhibitorUnbiased functional screenCheckpoint responseScreen identifiesCancer Genome AtlasFunctional screenGlioblastoma patient specimensMolecular networksGlioblastoma datasetGlioblastoma cellsGenome AtlasSystematic identificationGlioblastoma radioresistanceTherapeutic resistanceMiR125aRadioresistanceTGFβNew roleTGFβ inhibitorsTherapeutic applicationsGlioblastomaMIR1MiR150
2012
miR-1 and miR-206 regulate angiogenesis by modulating VegfA expression in zebrafish
Stahlhut C, Suárez Y, Lu J, Mishima Y, Giraldez AJ. miR-1 and miR-206 regulate angiogenesis by modulating VegfA expression in zebrafish. Development 2012, 139: 4356-4365. PMID: 23132244, PMCID: PMC3509730, DOI: 10.1242/dev.083774.Peer-Reviewed Original ResearchConceptsMiR-1/206Post-transcriptional modulatorsMiRNA-target interactionsMiR-1Appropriate physiological responsesRegulation of VEGFAZebrafish developmentEmbryonic developmentTarget protectorNovel functionPrecise regulationGene expressionMorphogenetic activityDevelopmental angiogenesisPutative targetsRegulate angiogenesisEssential processMiR-206Physiological responsesCellular communicationVEGFA expressionGrowth factorVascular endothelial growth factorExpressionAngiogenesisBlockade of miR-150 Maturation by MLL-Fusion/MYC/LIN-28 Is Required for MLL-Associated Leukemia
Jiang X, Huang H, Li Z, Li Y, Wang X, Gurbuxani S, Chen P, He C, You D, Zhang S, Wang J, Arnovitz S, Elkahloun A, Price C, Hong GM, Ren H, Kunjamma RB, Neilly MB, Matthews JM, Xu M, Larson RA, Le Beau MM, Slany RK, Liu PP, Lu J, Zhang J, He C, Chen J. Blockade of miR-150 Maturation by MLL-Fusion/MYC/LIN-28 Is Required for MLL-Associated Leukemia. Cancer Cell 2012, 22: 524-535. PMID: 23079661, PMCID: PMC3480215, DOI: 10.1016/j.ccr.2012.08.028.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorCell Transformation, NeoplasticDNA MethylationDown-RegulationFms-Like Tyrosine Kinase 3Gene DosageGene Expression Regulation, LeukemicHistone-Lysine N-MethyltransferaseHomeodomain ProteinsHumansLeukemiaMiceMicroRNAsMutationMyeloid Ecotropic Viral Integration Site 1 ProteinMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsNuclear ProteinsProto-Oncogene Proteins c-mycRNA-Binding ProteinsSignal TransductionConceptsMiR-150MiR-150 functionsLeukemic cell growthPathogenesis of leukemiaHoxa9/Meis1Acute leukemiaDysregulation of miRNAsExpression of microRNAsPivotal gatekeeperLeukemiaFunctional axisCell growthLeukemogenesisMYC/MLL fusion proteinsBlockadePathogenesisPosttranscriptional levelExpressionFusion proteinFLT3
2008
ADAR1 is essential for the maintenance of hematopoiesis and suppression of interferon signaling
Hartner JC, Walkley CR, Lu J, Orkin SH. ADAR1 is essential for the maintenance of hematopoiesis and suppression of interferon signaling. Nature Immunology 2008, 10: 109-115. PMID: 19060901, PMCID: PMC2701568, DOI: 10.1038/ni.1680.Peer-Reviewed Original Research
2003
An adenosine analogue, IB-MECA, down-regulates estrogen receptor alpha and suppresses human breast cancer cell proliferation.
Lu J, Pierron A, Ravid K. An adenosine analogue, IB-MECA, down-regulates estrogen receptor alpha and suppresses human breast cancer cell proliferation. Cancer Research 2003, 63: 6413-23. PMID: 14559831.Peer-Reviewed Original ResearchConceptsEstrogen receptor alphaIB-MECAMCF-7 cellsReceptor alphaHuman breast cancer cell proliferationBreast cancer cell proliferationDifferent adenosine analoguesHuman breast cancer cell line MCF-7Overexpression of ERalphaBreast cancer cell line MCF-7Breast cancer treatmentCancer cell line MCF-7Adenosine analoguesHs578T cellsCancer cell proliferationCell line MCF-7Breast cancer cell typesDifferent breast cancer cell typesCancer cell typesT cellsDrug treatmentN-methyluronamideSelective agonistZR-75Positive cells