2013
The Imprinted H19 LncRNA Antagonizes Let-7 MicroRNAs
Kallen AN, Zhou XB, Xu J, Qiao C, Ma J, Yan L, Lu L, Liu C, Yi JS, Zhang H, Min W, Bennett AM, Gregory RI, Ding Y, Huang Y. The Imprinted H19 LncRNA Antagonizes Let-7 MicroRNAs. Molecular Cell 2013, 52: 101-112. PMID: 24055342, PMCID: PMC3843377, DOI: 10.1016/j.molcel.2013.08.027.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesCell DifferentiationComputational BiologyDatabases, GeneticGene Expression ProfilingGene Expression RegulationGenomic ImprintingGenotypeHEK293 CellsHuman Umbilical Vein Endothelial CellsHumansMiceMicroRNAsMuscle DevelopmentMyoblasts, SkeletalPhenotypeRibonucleoproteinsRNA InterferenceRNA, Long NoncodingTime FactorsTransfectionConceptsLet-7 familyWide transcriptome analysisHuman genetic disordersNoncanonical binding siteLet-7 microRNALet-7 overexpressionGene functionH19 depletionTranscriptome analysisMuscle differentiationMolecular spongeUnexpected modeImportant regulatorAdult muscleH19 knockdownRecent implicationMiR-675Physiological significanceMicroRNAsH19Binding sitesGenetic disordersOverexpressionImportant roleFetal tissues
2012
Both Internalization and AIP1 Association Are Required for Tumor Necrosis Factor Receptor 2-Mediated JNK Signaling
Ji W, Li Y, Wan T, Wang J, Zhang H, Chen H, Min W. Both Internalization and AIP1 Association Are Required for Tumor Necrosis Factor Receptor 2-Mediated JNK Signaling. Arteriosclerosis Thrombosis And Vascular Biology 2012, 32: 2271-2279. PMID: 22743059, PMCID: PMC3421067, DOI: 10.1161/atvbaha.112.253666.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBinding SitesCells, CulturedEndothelial CellsEnzyme ActivationHuman Umbilical Vein Endothelial CellsHumansJNK Mitogen-Activated Protein KinasesMiceMice, KnockoutNF-kappa BProtein Interaction Domains and MotifsProtein TransportRas GTPase-Activating ProteinsReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISequence DeletionSignal TransductionTime FactorsTNF Receptor-Associated Factor 2TransfectionTumor Necrosis Factor-alphaConceptsJNK signalingApoptotic signalingJNK activationDomain IICaspase-dependent cell deathCell deathTNF receptor 1C-Jun N-terminal kinaseDependent cell survivalNF-κB activationN-terminal kinaseNF-κBDeletion analysisTNF responseLL motifPlasma membraneIntracellular regionCell survivalDomain IJNKSignalingDistinct rolesTNFR2 deletionProtein 1Specific deletion
2011
AIP1 Prevents Graft Arteriosclerosis by Inhibiting Interferon-&ggr;–Dependent Smooth Muscle Cell Proliferation and Intimal Expansion
Yu L, Qin L, Zhang H, He Y, Chen H, Pober JS, Tellides G, Min W. AIP1 Prevents Graft Arteriosclerosis by Inhibiting Interferon-&ggr;–Dependent Smooth Muscle Cell Proliferation and Intimal Expansion. Circulation Research 2011, 109: 418-427. PMID: 21700930, PMCID: PMC3227522, DOI: 10.1161/circresaha.111.248245.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAorta, AbdominalAorta, ThoracicArteriosclerosisCell MovementCell ProliferationCells, CulturedDisease Models, AnimalHumansInterferon-gammaJanus Kinase 2MaleMiceMice, KnockoutMinor Histocompatibility AntigensMuscle, Smooth, VascularRas GTPase-Activating ProteinsReceptors, InterferonSignal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorTime FactorsTunica IntimaVascular GraftingConceptsASK1-interacting protein-1Neointima formationTransplantation modelIntimal expansionSingle minor histocompatibility antigenSmooth muscle cell proliferationMinor histocompatibility antigensAortic transplantation modelAorta transplantation modelMuscle cell proliferationVSMC accumulationDonor graftsGraft arteriosclerosisIntimal formationIntravenous administrationHistocompatibility antigensVSMC proliferationMouse aortaVSMC migrationIFNProliferative diseasesEndothelial cellsProtein 1Cell proliferationJAK-STAT signaling
2010
Endothelial-Specific Transgenesis of TNFR2 Promotes Adaptive Arteriogenesis and Angiogenesis
Luo Y, Xu Z, Wan T, He Y, Jones D, Zhang H, Min W. Endothelial-Specific Transgenesis of TNFR2 Promotes Adaptive Arteriogenesis and Angiogenesis. Arteriosclerosis Thrombosis And Vascular Biology 2010, 30: 1307-1314. PMID: 20395596, PMCID: PMC2889154, DOI: 10.1161/atvbaha.110.204222.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsApoptosisCell ProliferationCell SurvivalDisease Models, AnimalEndothelial CellsFemoral ArteryHindlimbHumansIschemiaLigationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMuscle, SkeletalNeovascularization, PhysiologicProtein-Tyrosine KinasesReceptors, Tumor Necrosis Factor, Type IIRecovery of FunctionRegional Blood FlowTime FactorsVascular Endothelial Growth Factor Receptor-2ConceptsFemoral artery ligation modelIschemic reserve capacityLimb perfusion recoveryTNFR2-deficient micePeripheral arterial diseaseCoronary artery diseaseIschemia-induced angiogenesisArtery ligation modelTNFR2 knockoutTNFR2-KOArtery diseaseActivation of TNFR2Adaptive angiogenesisArterial diseaseTg miceVascular diseaseLigation modelPerfusion recoveryAdaptive arteriogenesisVascular endotheliumLower limbsUpper limbGlobal deletionTNFR2Mice
2009
Endothelial-Specific Expression of Mitochondrial Thioredoxin Promotes Ischemia-Mediated Arteriogenesis and Angiogenesis
Dai S, He Y, Zhang H, Yu L, Wan T, Xu Z, Jones D, Chen H, Min W. Endothelial-Specific Expression of Mitochondrial Thioredoxin Promotes Ischemia-Mediated Arteriogenesis and Angiogenesis. Arteriosclerosis Thrombosis And Vascular Biology 2009, 29: 495-502. PMID: 19150880, PMCID: PMC2734510, DOI: 10.1161/atvbaha.108.180349.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisArteriesBlood Flow VelocityCell MovementDisease Models, AnimalEndothelial CellsHindlimbIschemiaJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Kinase Kinase 5MiceMice, TransgenicMitochondriaMuscle, SkeletalNeovascularization, PhysiologicNitric OxideOxidative StressReactive Oxygen SpeciesRegional Blood FlowSignal TransductionThioredoxinsTime FactorsConceptsEndothelial cellsFlow recoveryFemoral artery ligation modelIschemia-mediated arteriogenesisIschemic reserve capacityLimb perfusion recoveryENOS-deficient miceENOS-KO miceNitric oxide bioavailabilityIschemia-induced angiogenesisEC apoptosisArtery ligation modelEC survivalENOS deletionNontransgenic littermatesStress-induced activationLigation modelPerfusion recoveryLower limbsUpper limbEndothelial-specific expressionSevere impairmentMajor antioxidant proteinsIschemiaMice
2008
SENP1 mediates TNF-induced desumoylation and cytoplasmic translocation of HIPK1 to enhance ASK1-dependent apoptosis
Li X, Luo Y, Yu L, Lin Y, Luo D, Zhang H, He Y, Kim YO, Kim Y, Tang S, Min W. SENP1 mediates TNF-induced desumoylation and cytoplasmic translocation of HIPK1 to enhance ASK1-dependent apoptosis. Cell Death & Differentiation 2008, 15: 739-750. PMID: 18219322, DOI: 10.1038/sj.cdd.4402303.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcysteineAnimalsAntioxidantsApoptosisCarrier ProteinsCattleCells, CulturedCysteine EndopeptidasesCytoplasmEndopeptidasesEndothelial CellsFibroblastsHumansMAP Kinase Kinase Kinase 5MiceMice, KnockoutMutationProtein KinasesProtein Processing, Post-TranslationalProtein Serine-Threonine KinasesProtein TransportReactive Oxygen SpeciesRecombinant ProteinsRNA InterferenceRNA, Small InterferingSignal TransductionSmall Ubiquitin-Related Modifier ProteinsThioredoxinsTime FactorsTransfectionTumor Necrosis Factor-alphaConceptsASK1-dependent apoptosisASK1-JNK activationCytoplasmic translocationMouse embryonic fibroblast cellsNuclear translocationSUMO-specific proteasesWild-type formEmbryonic fibroblast cellsNuclear importAntioxidant protein thioredoxinHIPK1Mutant formsEndothelial cellsDeSUMOylationProtein thioredoxinSubsequent cytoplasmic translocationSENP1TranslocationCritical functionsThioredoxinFibroblast cellsApoptosisCellsActivationSUMO