2010
Stabilization of VEGFR2 Signaling by Cerebral Cavernous Malformation 3 Is Critical for Vascular Development
He Y, Zhang H, Yu L, Gunel M, Boggon TJ, Chen H, Min W. Stabilization of VEGFR2 Signaling by Cerebral Cavernous Malformation 3 Is Critical for Vascular Development. Science Signaling 2010, 3: ra26. PMID: 20371769, PMCID: PMC3052863, DOI: 10.1126/scisignal.2000722.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCardiovascular SystemEndothelial CellsFluorescent Antibody Technique, IndirectGene DeletionGene Expression ProfilingGene Knockdown TechniquesHematopoiesisHumansImmunoblottingImmunohistochemistryImmunoprecipitationMiceReverse Transcriptase Polymerase Chain ReactionSignal TransductionVascular Endothelial Growth Factor Receptor-2ConceptsCarboxyl-terminal domainVascular endothelial growth factor receptor 2Vascular developmentHuman vascular malformationsCerebral cavernous malformation 3Early embryonic stagesCerebral cavernous malformationsEndothelial cell-specific deletionApoptotic stimuliCell-specific deletionVivo functionEmbryonic angiogenesisEndothelial growth factor receptor 2Unknown functionVEGF stimulationVEGFR2 signalingEmbryonic stagesMessenger RNASmooth muscle cellsGrowth factor receptor 2DeletionCCM3 genesFactor receptor 2Muscle cellsGenesRole of DAB2IP in modulating epithelial-to-mesenchymal transition and prostate cancer metastasis
Xie D, Gore C, Liu J, Pong RC, Mason R, Hao G, Long M, Kabbani W, Yu L, Zhang H, Chen H, Sun X, Boothman DA, Min W, Hsieh JT. Role of DAB2IP in modulating epithelial-to-mesenchymal transition and prostate cancer metastasis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 2485-2490. PMID: 20080667, PMCID: PMC2823864, DOI: 10.1073/pnas.0908133107.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta CateninBlotting, WesternCadherinsCell LineCell Line, TumorCell MovementEpithelial CellsGene ExpressionHumansImmunohistochemistryMaleMesodermMiceMice, NudeNeoplasm MetastasisNeoplasms, ExperimentalProstatic NeoplasmsRas GTPase-Activating ProteinsReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingTCF Transcription FactorsTransfectionTransplantation, HeterologousVimentinConceptsProstate cancerMesenchymal transitionDAB2IP expressionCarcinoma cellsMultiple lymph nodesMetastatic prostate cancerDistant organ metastasisAggressive prostate cancerMetastatic PCa cellsProstate cancer metastasisClinical prostate cancer specimensHuman normal prostatePotential therapeutic targetXenograft mouse modelProstate cancer specimensProstate carcinoma cellsLymph nodesOrgan metastasisPCa cellsRole of DAB2IPPrognostic biomarkerPCa metastasisKnockout miceTherapeutic targetHuman carcinoma cells
2007
Endothelial-Specific Expression of Mitochondrial Thioredoxin Improves Endothelial Cell Function and Reduces Atherosclerotic Lesions
Zhang H, Luo Y, Zhang W, He Y, Dai S, Zhang R, Huang Y, Bernatchez P, Giordano FJ, Shadel G, Sessa WC, Min W. Endothelial-Specific Expression of Mitochondrial Thioredoxin Improves Endothelial Cell Function and Reduces Atherosclerotic Lesions. American Journal Of Pathology 2007, 170: 1108-1120. PMID: 17322393, PMCID: PMC1864879, DOI: 10.2353/ajpath.2007.060960.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaApolipoproteins EAtherosclerosisCells, CulturedEndothelial CellsFlow CytometryImmunoblottingImmunohistochemistryMiceMice, TransgenicMicroscopy, ConfocalMitochondrial ProteinsNitric OxideReactive Oxygen SpeciesReverse Transcriptase Polymerase Chain ReactionThioredoxinsVasodilationConceptsTg miceAtherosclerotic lesionsOxidative stressNitric oxide levelsEC functionDeficient mouse modelEndothelial cell functionAtherosclerosis developmentEnhanced vasodilationVascular EC functionEndothelium functionApolipoprotein EControl littermatesMouse modelOxide levelsMice showCapacity of ECEndothelial-specific expressionEndothelial cellsCritical roleReactive oxygen speciesCell functionMiceTotal antioxidantsLesions