2007
RIP1-mediated AIP1 Phosphorylation at a 14-3-3-binding Site Is Critical for Tumor Necrosis Factor-induced ASK1-JNK/p38 Activation*
Zhang R, Zhang H, Lin Y, Li J, Pober JS, Min W. RIP1-mediated AIP1 Phosphorylation at a 14-3-3-binding Site Is Critical for Tumor Necrosis Factor-induced ASK1-JNK/p38 Activation*. Journal Of Biological Chemistry 2007, 282: 14788-14796. PMID: 17389591, DOI: 10.1074/jbc.m701148200.Peer-Reviewed Original ResearchMeSH Keywords14-3-3 ProteinsAdaptor Proteins, Signal TransducingAmino Acid SubstitutionAnimalsApoptosisCarrier ProteinsCattleCells, CulturedEndothelial CellsEnzyme ActivationGuanylate KinasesHumansMAP Kinase Kinase 4MAP Kinase Kinase Kinase 5MAP Kinase Signaling SystemMultiprotein ComplexesMutation, MissenseP38 Mitogen-Activated Protein KinasesPhosphorylationProtein BindingProtein Processing, Post-TranslationalProteinsReceptor-Interacting Protein Serine-Threonine KinasesTNF Receptor-Associated Factor 2Tumor Necrosis Factor-alphaConceptsJNK/p38 activationP38 activationTRAF2-ASK1ASK1-JNK activationPhospho-specific antibodiesTNF treatmentEndothelial cellsComplex formationGAP domainProtein familyTerminal domainAIP1Novel memberApoptotic signalingTNF signalingRNA knockdownRIP1PhosphorylationProtein 1ASK1-interacting protein-1EC apoptosisTRAF2ASK1Similar kineticsTumor necrosis factor
2006
Differential Functions of Tumor Necrosis Factor Receptor 1 and 2 Signaling in Ischemia-Mediated Arteriogenesis and Angiogenesis
Luo D, Luo Y, He Y, Zhang H, Zhang R, Li X, Dobrucki WL, Sinusas AJ, Sessa WC, Min W. Differential Functions of Tumor Necrosis Factor Receptor 1 and 2 Signaling in Ischemia-Mediated Arteriogenesis and Angiogenesis. American Journal Of Pathology 2006, 169: 1886-1898. PMID: 17071609, PMCID: PMC1780200, DOI: 10.2353/ajpath.2006.060603.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsArteriesBlood VesselsCattleCell MovementCell ProliferationCell SurvivalEndothelial CellsEndothelium, VascularHindlimbHumansIschemiaMiceMice, Inbred C57BLMice, KnockoutMolecular Sequence DataNeovascularization, PathologicOrganogenesisPerfusionProtein-Tyrosine KinasesReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISignal TransductionTNF Receptor-Associated Factor 2ConceptsTNFR2 KO miceTumor necrosis factorTNFR1-KOEndothelial cellsFemoral artery ligation modelIschemia-mediated arteriogenesisIschemic reserve capacityTNFR1 knockout miceInfiltration of macrophagesTumor necrosis factor receptor 1Wild-type miceArtery ligation modelNecrosis factor receptor 1Dependent reporter gene expressionNuclear factor-kappaBEC survivalFactor receptor 1Vascular endothelial cellsActivation of TNFR1Murine endothelial cellsTNFR2-KOClinical recoveryActivation of TNFR2Limb perfusionVascular proliferationSOCS1 Inhibits Tumor Necrosis Factor-induced Activation of ASK1-JNK Inflammatory Signaling by Mediating ASK1 Degradation*
He Y, Zhang W, Zhang R, Zhang H, Min W. SOCS1 Inhibits Tumor Necrosis Factor-induced Activation of ASK1-JNK Inflammatory Signaling by Mediating ASK1 Degradation*. Journal Of Biological Chemistry 2006, 281: 5559-5566. PMID: 16407264, DOI: 10.1074/jbc.m512338200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCattleCells, CulturedEndothelial CellsEnzyme ActivationInflammationIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 5MiceMice, KnockoutRecombinant Fusion ProteinsRepressor ProteinsSignal TransductionSrc Homology DomainsSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTumor Necrosis Factor-alphaConceptsASK1 degradationDissociation of ASK1Member of suppressorTumor necrosis factor-induced activationEndothelial cellsActivation of JNKPhosphotyrosine bindingUndergoes ubiquitinationSH2 domainProteasomal inhibitorsASK1 activationNegative regulatorApoptotic responseASK1Cytokine signalingSOCS1 functionsASK1 expressionSOCS1Tumor necrosis factorSignalingSOCS1-deficient mice