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
2009
DAB2IP coordinates both PI3K-Akt and ASK1 pathways for cell survival and apoptosis
Xie D, Gore C, Zhou J, Pong RC, Zhang H, Yu L, Vessella RL, Min W, Hsieh JT. DAB2IP coordinates both PI3K-Akt and ASK1 pathways for cell survival and apoptosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 19878-19883. PMID: 19903888, PMCID: PMC2785260, DOI: 10.1073/pnas.0908458106.Peer-Reviewed Original ResearchConceptsDAB2IP proteinCell survivalDeath-signaling moleculePI3K-Akt activityPI3K-Akt activationMetastatic prostate cancer cellsPI3K-Akt pathwayCell cycle arrestASK1 activityScaffold proteinPotent growth inhibitorDeath signalsC2 domainSignal moleculesASK1 activationFunctional analysisCell homeostasisApoptotic defectsConstitutive activationJNK pathwayProstate cancer cellsASK1 pathwayPI3K-AktDAB2IP expressionCycle arrest