2016
FADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis
Ranjan K, Pathak C. FADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis. Scientific Reports 2016, 6: 22787. PMID: 26972597, PMCID: PMC4789601, DOI: 10.1038/srep22787.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsApoptosisBaculoviral IAP Repeat-Containing 3 ProteinBlotting, WesternCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Cell LineCell SurvivalFas-Associated Death Domain ProteinHCT116 CellsHEK293 CellsHeLa CellsHT29 CellsHumansInhibitor of Apoptosis ProteinsMCF-7 CellsMiceNF-kappa BNIH 3T3 CellsProtein BindingRepressor ProteinsRNA InterferenceTumor Necrosis Factor-alphaUbiquitin-Protein LigasesUbiquitinationConceptsCell deathProcaspase-8Molecular mechanismsCellular FLICE-like inhibitory proteinFLICE-like inhibitory proteinExpression of cFLIPLCell death signalingApoptosis protein 2Apoptotic cell death signalingHEK 293T cellsNovel molecular mechanismApoptotic cell deathNF-κB activationFasL stimulationCellular inhibitorE3 ubiquitinTNF-α stimulationDeath domainDeath inducingDeath signalingEctopic expressionFADDCaspase-8NF-κBCell survival
2015
Genetic variants associated with autoimmunity drive NFκB signaling and responses to inflammatory stimuli
Housley WJ, Fernandez SD, Vera K, Murikinati SR, Grutzendler J, Cuerdon N, Glick L, De Jager PL, Mitrovic M, Cotsapas C, Hafler DA. Genetic variants associated with autoimmunity drive NFκB signaling and responses to inflammatory stimuli. Science Translational Medicine 2015, 7: 291ra93. PMID: 26062845, PMCID: PMC4574294, DOI: 10.1126/scitranslmed.aaa9223.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAllelesAutoimmunityCase-Control StudiesCD4-Positive T-LymphocytesCell NucleusCytokinesFemaleGenetic Predisposition to DiseaseHumansInflammationMaleMiddle AgedMultiple SclerosisNF-kappa BPolymorphism, Single NucleotideProtein TransportReceptors, Tumor Necrosis Factor, Type IRisk FactorsSex CharacteristicsSignal TransductionTime FactorsTumor Necrosis Factor-alphaConceptsB-cell leukemia 3Multiple sclerosisNegative regulatorInflammatory stimuliGenetic variantsWide association studyDisease susceptibility variantsNaïve CD4 T cellsRapid genetic screeningCD4 T cellsActivation of p65Transcription factor nuclear factor κBExpression of NFκBNuclear factor κBApoptosis 1Cellular inhibitorGG risk genotypeDegradation of inhibitorCentral regulatorAssociation studiesCytokine blockadeUlcerative colitisAutoimmune diseasesTumor necrosisSusceptibility variants
2006
Evaluation of the Prognostic Value of Cellular Inhibitor of Apoptosis Protein in Epithelial Ovarian Cancer Using Automated Quantitative Protein Analysis
Psyrri A, Yu Z, Bamias A, Weinberger PM, Markakis S, Kowalski D, Camp RL, Rimm DL, Dimopoulos MA. Evaluation of the Prognostic Value of Cellular Inhibitor of Apoptosis Protein in Epithelial Ovarian Cancer Using Automated Quantitative Protein Analysis. Cancer Epidemiology Biomarkers & Prevention 2006, 15: 1179-1183. PMID: 16775178, DOI: 10.1158/1055-9965.epi-06-0120.Peer-Reviewed Original ResearchConceptsEpithelial ovarian cancerOvarian cancerPrognostic valuePaclitaxel-based combination chemotherapyOnly significant prognostic factorAdvanced stage ovarian cancerSignificant prognostic factorsOvarian cancer patientsProtein levelsImportant prognostic biomarkerMean followSurgical debulkingCombination chemotherapyOverall survivalPrognostic factorsClinical outcomesMultivariable analysisEntire cohortCancer patientsPrognostic biomarkerPrognostic variablesMembranous expressionApoptosis proteinSurvival rateCellular inhibitor
2003
Phospholipids Can Switch the GTPase Substrate Preference of a GTPase-activating Protein*
Ligeti E, Dagher MC, Hernandez SE, Koleske AJ, Settleman J. Phospholipids Can Switch the GTPase Substrate Preference of a GTPase-activating Protein*. Journal Of Biological Chemistry 2003, 279: 5055-5058. PMID: 14699145, DOI: 10.1074/jbc.c300547200.Peer-Reviewed Original ResearchConceptsGTPase-activating proteinsSmall GTPasesSubstrate preferencePotent GTPase-activating proteinMajor cellular inhibitorActivity of GTPasesNovel regulatory mechanismLikely physiological roleRacGAP activityIntrinsic GTPRhoGAP activityP190 RhoGAPCellular inhibitorRac GTPasesGTPasesRegulatory mechanismsPhysiological roleProteinPhospholipidsFatty acidsRhoGAPGTPP190ActivityRho
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