Search results for "CASP"

showing 10 items of 470 documents

Colony-stimulating factor-1-induced oscillations in phosphatidylinositol-3 kinase/AKT are required for caspase activation in monocytes undergoing dif…

2009

Abstract The differentiation of human peripheral blood monocytes into resident macrophages is driven by colony-stimulating factor-1 (CSF-1), which upon interaction with CSF-1 receptor (CSF-1R) induces within minutes the phosphorylation of its cytoplasmic tyrosine residues and the activation of multiple signaling complexes. Caspase-8 and -3 are activated at day 2 to 3 and contribute to macrophage differentiation, for example, through cleavage of nucleophosmin. Here, we show that the phosphatidylinositol-3 kinase and the downstream serine/threonine kinase AKT connect CSF-1R activation to caspase-8 cleavage. Most importantly, we demonstrate that successive waves of AKT activation with increasi…

Macrophage colony-stimulating factorCellular differentiationImmunologyImmunoblottingApoptosisBiologyBiochemistryMonocytesImmunoenzyme TechniquesPhosphatidylinositol 3-KinasesHumansImmunoprecipitationRNA MessengerPhosphorylationProtein kinase BCells CulturedPhosphoinositide-3 Kinase InhibitorsMitogen-Activated Protein Kinase 1Caspase 8Mitogen-Activated Protein Kinase 3MAP kinase kinase kinaseKinaseAkt/PKB signaling pathwayReverse Transcriptase Polymerase Chain ReactionMacrophage Colony-Stimulating FactorMacrophagesCell DifferentiationCell BiologyHematologyFlow CytometryCell biologyEnzyme ActivationPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionBlood
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Fine-tuning nucleophosmin in macrophage differentiation and activation

2011

Abstract M-CSF–driven differentiation of peripheral blood monocytes is one of the sources of tissue macrophages. In humans and mice, the differentiation process involves the activation of caspases that cleave a limited number of proteins. One of these proteins is nucleophosmin (NPM1), a multifunctional and ubiquitous protein. Here, we show that caspases activated in monocytes exposed to M-CSF cleave NPM1 at D213 to generate a 30-kDa N-terminal fragment. The protein is further cleaved into a 20-kDa fragment, which involves cathepsin B. NPM1 fragments contribute to the limited motility, migration, and phagocytosis capabilities of resting macrophages. Their activation with lipopolysaccharides …

Macrophage colony-stimulating factorLipopolysaccharidesCellular differentiationImmunologyBiochemistryProinflammatory cytokine03 medical and health sciencesPhagocytes Granulocytes and MyelopoiesisMice0302 clinical medicineAnimalsHumansNuclear proteinCaspaseCells Cultured030304 developmental biologyMice Knockout0303 health sciencesNucleophosminbiologyMacrophage Colony-Stimulating FactorMacrophagesNuclear ProteinsCell DifferentiationCell BiologyHematologyMacrophage ActivationNFKB1Molecular biologyCathepsinsCell biologyProtein Structure TertiaryCXCL1Mice Inbred C57BL030220 oncology & carcinogenesisCaspasesbiology.proteinNucleophosminProtein Processing Post-TranslationalBlood
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Incidence and risk factors of post-engraftment invasive fungal disease in adult allogeneic hematopoietic stem cell transplant recipients receiving or…

2015

Studies that analyze the epidemiology and risk factors for invasive fungal disease (IFD) after engraftment in alloSCT are few in number. This single-center retrospective study included 404 alloSCT adult recipients surviving > 40 days who engrafted and were discharged without prior IFD. All patients who received >= 20 mg/day of prednisone were assigned to primary oral prophylaxis (itraconazole or low-dose voriconazole). The primary end point was the cumulative incidence (CI) of probable/proven IFD using the European Organization for Research and Treatment of Cancer and Mycoses Study Group (EORTC/MSG) criteria. The independent prognostic factors after multivariate analyses were used to constr…

MaleAntifungal AgentsTransplantation ConditioningPremedicationmedicine.medical_treatmentMULTICENTERAdministration OralHematopoietic stem cell transplantationEchinocandinsCOMPETING RISKCaspofunginRisk FactorsCause of DeathINFECTIONGranulocyte Colony-Stimulating FactorEPIDEMIOLOGYCumulative incidenceTreatment FailureFramingham Risk ScoreIncidenceIncidence (epidemiology)Hematopoietic Stem Cell TransplantationHematologyMiddle AgedAllograftsHematologic NeoplasmsVORICONAZOLEDrug Therapy CombinationFemaleASPERGILLOSISRisk assessmentFungemiamedicine.drugAdultmedicine.medical_specialtyNeutropeniaANTIFUNGAL PROPHYLAXISNeutropeniaRisk AssessmentITRACONAZOLEMedication AdherenceImmunocompromised HostLipopeptidesYoung AdultAmphotericin BInternal medicinemedicineAspergillosisHumansAgedRetrospective StudiesVoriconazoleTransplantationbusiness.industryRetrospective cohort studyFLUCONAZOLETriazolesmedicine.diseaseSurvival AnalysisSurgeryMycosesPatient CompliancebusinessSCT
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Inhibition of DNA methylation sensitizes glioblastoma for tumor necrosis factor-related apoptosis-inducing ligand-mediated destruction.

2005

AbstractLife expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability to kill glioma cell lines in vitro and in vivo. Here, we show that, differently from glioma cell lines, glioblastoma multiforme tumors were resistant to TRAIL stimulation because they expressed low levels of caspase-8 and high levels of the death receptor inhibitor PED/PEA-15. Inhibition of methyltransferases by decitabine resulted in considerable up-regulation of TRAIL receptor-1 and caspase-8, down-regulation of PED/PEA-15, inhibition of cell growth, and …

MaleCancer ResearchMethyltransferaseNudeDrug ResistanceApoptosisReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandCASPASE-8 EXPRESSIONMiceNude mouseSIGNALING COMPLEXReceptorsAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedDNA Modification MethylasesIN-VIVOHeterologousCaspase 8CulturedMembrane GlycoproteinsbiologyIntracellular Signaling Peptides and ProteinsMiddle AgedTumor CellsGene Expression Regulation NeoplasticMALIGNANT GLIOMA-CELLSOncologyCaspasesDNA methylationAzacitidineTumor necrosis factor alphaFemalemedicine.drugSignal TransductionAdultBRAIN-TUMORSTransplantation HeterologousCHEMOTHERAPEUTIC-AGENTSDecitabineMice NudeDecitabineDRUG-INDUCED APOPTOSISDEATH RECEPTOR5-AZA-2'-DEOXYCYTIDINEIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansneoplasmsAgedTransplantationNeoplasticCell growthTumor Necrosis Factor-alphaHistocompatibility Antigens Class IDNA Methylationbiology.organism_classificationPhosphoproteinsReceptors TNF-Related Apoptosis-Inducing LigandGene Expression RegulationApoptosisDrug Resistance NeoplasmImmunologyCancer researchNeoplasmAdult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulatory Proteins; Azacitidine; Caspase 8; Caspases; DNA Modification Methylases; Drug Resistance Neoplasm; Female; Glioblastoma; Histocompatibility Antigens Class I; Humans; Intracellular Signaling Peptides and Proteins; Male; Membrane Glycoproteins; Mice; Mice Nude; Middle Aged; Phosphoproteins; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor Cells Cultured; Tumor Necrosis Factor-alpha; DNA Methylation; Gene Expression Regulation Neoplastic; Cancer Research; OncologyTumor Necrosis FactorTRAIL-INDUCED APOPTOSISApoptosis Regulatory ProteinsGlioblastomaCancer research
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The associated expression of Maspin and Bax proteins as a potential prognostic factor in intrahepatic cholangiocarcinoma

2006

Abstract Background Maspin, a member of the serpin family, is a suppressor of tumor growth, an inhibitor of angiogenesis and an inducer of apoptosis. Maspin induces apoptosis by increasing Bax, a member of the Bcl-2 family of apoptosis-regulating proteins. In this exploratory study, we investigated the associated expression of Maspin and Bax proteins as a potential prognostic factor in intrahepatic cholangiocarcinoma (IHCCA). Methods Twenty-two paraffin-embedded samples were analyzed by immunohistochemical methods using Maspin, Bax and CD34 antibodies. Maspin was scored semiquantitatively (HSCORE). Apoptosis was assessed using an antibody against cleaved caspase-3. Results The strong relati…

MaleCancer ResearchPathologymedicine.medical_specialtyAngiogenesisApoptosisCaspase 3Kaplan-Meier EstimateSerpinlcsh:RC254-282law.inventionCholangiocarcinomaBcl-2-associated X proteinlawBiomarkers TumorGeneticsmedicineHumansGenes Tumor SuppressorSerpinsIntrahepatic CholangiocarcinomaAgedbcl-2-Associated X ProteinbiologyCaspase 3business.industryMicrocirculationLiver NeoplasmsMaspinMiddle AgedPrognosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsEnzyme ActivationOncologyApoptosisCancer researchbiology.proteinSuppressorFemalebusinessResearch ArticleBMC Cancer
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Pyrrolotetrazinones deazaanalogues of temozolomide induce apoptosis in Jurkat cell line: involvement of tubulin polymerization inhibition.

2009

Pyrrolotetrazinones are a new class of azolotetrazinones endowed with a high, remarkable antiproliferative activity in human tumor cultured cells. They hold the deaza skeleton of the antitumor drug temozolomide, although preliminary investigations indicated a different mechanism of action. To understand their mechanism(s) of action along with their target at molecular level, four derivatives were selected on the basis of their activity on a panel of human tumor cell lines and they were investigated in depth in a T leukemia cell line (Jurkat). Flow cytometric analysis of cell cycle after treatment with pyrrolotetrazinones has demonstrated that they were able to induce an arrest of the cell c…

MaleCancer ResearchProgrammed cell deathCarcinoma HepatocellularCell SurvivalCellGene ExpressionAntineoplastic AgentsApoptosisPhosphatidylserinesBiologyToxicologyJurkat cellsMicrotubulesMicrotubule polymerizationJurkat CellsMiceTubulinCell Line TumormedicineTemozolomideAnimalsHumansPharmacology (medical)Cell Proliferationbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialMice Inbred BALB CCaspase 3Cell CycleCell MembraneCell cycleSettore CHIM/08 - Chimica FarmaceuticaTubulin ModulatorsCell biologyMitochondriaDacarbazinemedicine.anatomical_structureOncologyMechanism of actionBiochemistryProto-Oncogene Proteins c-bcl-2ApoptosisCell culturemedicine.symptomPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesPyrrolotetrazinoneCancer chemotherapy and pharmacology
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Up-regulation of c-FLIPshort and reduction of activation-induced cell death in T-cells from patients with Type 1 diabetes

2004

AICD of T-cells is an efficient way of removing activated T-lymphocytes. In this study we investigated the molecular basis of AICD upon reactivation in peripheral T-lymphocytes from newly diagnosed T1DM patients and age-matched healthy controls. In an in vitro model system, PHA-stimulated T-cells, upon prolonged culture in IL-2, acquire a sensitive phenotype to Fas-mediated apoptosis. This phenomenon is less pronounced in T1DM T-cells. Moreover, the restimulation of activated T-cells via TCR/CD3 and/or via CD28 inhibits Fas-mediated apoptosis in T1DM in comparison to control T-cells. After Fas triggering, the generation of the active sub-units of caspase-8 is significantly reduced in T1DM T…

MaleCaspase 8Adolescenttype 1 diabetesT-LymphocytesCASP8 and FADD-Like Apoptosis Regulating ProteinIntracellular Signaling Peptides and ProteinsApoptosisLymphocyte ActivationCaspase InhibitorsSettore MED/13 - EndocrinologiaUp-RegulationDiabetes Mellitus Type 1CD28 AntigensReceptor-CD3 Complex Antigen T-CellCase-Control StudiesCaspasesHumansFemaleCarrier Proteins
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Evaluation of drug-metabolizing and functional competence of human hepatocytes incubated under hypothermia in different media for clinical infusion.

2008

Hepatocyte transplantation has been proposed as a method to support patients with liver insufficiency. Key factors for clinical cell transplantation to progress is to prevent hepatocyte damage, loss of viability and cell functionality, factors that depend on the nature of the tissue used for isolation to a large extent. The main sources of tissue for hepatocyte isolation are marginal livers that are unsuitable for transplantation, and segments from reduced cadaveric grafts. Hepatocellular transplantation requires infusing human hepatocytes in Suspension over a period of minutes to hours. The beneficial effect of hypothermic preservation of hepatocytes in infusion medium has been reported, b…

MaleCell Survivalmedicine.medical_treatmentCellBiomedical EngineeringCell Culture Techniqueslcsh:MedicineApoptosisBiologyPharmacologyRats Sprague-Dawleychemistry.chemical_compoundCytochrome P-450 Enzyme SystemmedicineCell AdhesionAnimalsHumansUreaViability assaySalineCells CulturedTransplantationGlycogenLiver Diseaseslcsh:RCell BiologyHyperthermia InducedHypothermiaAcetylcysteineCulture MediaRatsTransplantationmedicine.anatomical_structureGlucosechemistryApoptosisHepatocyteCaspasesInactivation MetabolicTissue TransplantationHepatocytesmedicine.symptomEnergy MetabolismCell transplantation
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Neuroprotective properties of mildronate, a mitochondria-targeted small molecule.

2010

Mildronate, a representative of the aza-butyrobetaine class of drugs with proven cardioprotective efficacy, was recently found to prevent dysfunction of complex I in rat liver mitochondria. The present study demonstrates that mildronate also acts as a neuroprotective agent. In a mouse model of azidothymidine (anti-HIV drug) neurotoxicity, mildronate reduced the azidothymidine-induced alterations in mouse brain tissue: it normalized the increase in caspase-3, cellular apoptosis susceptibility protein (CAS) and iNOS expression assessed by quantitative and semi-quantitative analysis. Mildronate also normalized the changes in cytochrome c oxidase (COX) expression, reduced the expression of glia…

MaleCell signalingAnti-HIV AgentsNitric Oxide Synthase Type IIMice Inbred StrainsMitochondrionPharmacologyNeuroprotectionElectron Transport Complex IVMiceCellular Apoptosis Susceptibility ProteinGlial Fibrillary Acidic ProteinmedicineAnimalsLymphocytesNeuroinflammationGlial fibrillary acidic proteinbiologyCaspase 3General NeuroscienceNeurodegenerationNeurotoxicityBrainmedicine.diseaseDisease Models AnimalNeuroprotective AgentsBiochemistrybiology.proteinNeurotoxicity SyndromesZidovudineCellular apoptosis susceptibility proteinMethylhydrazinesNeuroscience letters
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Acute ammonia neurotoxicity in vivo involves increase in cytoplasmic protein P53 without alterations in other markers of apoptosis.

2007

Acute intoxication with large ammonia doses leads to activation of NMDA receptors in the brain, resulting in oxidative stress and disturbance of mitochondrial function. Altered mitochondrial function is a crucial step in some mechanisms of cellular apoptosis. This study assesses whether ammonia intoxication in vivo leads to induction of apoptotic markers such as permeability transition pore (PTP) formation, caspase-3, and caspase-9 activation, changes in p53 protein, or cytochrome c release. Acute ammonia intoxication did not affect caspase-9 or caspase-3 activities. The mitochondrial membrane potential also remained unaltered in non-synaptic brain mitochondria after injection of ammonia, i…

MaleCytoplasmApoptosisMitochondrionmedicine.disease_causeCellular and Molecular NeuroscienceIn vivoAmmoniamedicineAnimalsRats WistarbiologyCaspase 3brain mitochondriaCytochrome capoptosisNeurotoxicityBrainCytochromes cammonia toxicitybrain nucleimedicine.diseaseCaspase 9Cell biologyMitochondriaRatsEnzyme ActivationCytosolcytochrome cCytoplasmApoptosisbiology.proteinTumor Suppressor Protein p53Oxidative stressJournal of neuroscience research
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