Search results for "caspases"

showing 10 items of 157 documents

JNK and AP-1 mediate apoptosis induced by bortezomib in HepG2 cells via FasL/caspase-8 and mitochondria-dependent pathways

2006

The proteasome inhibitor bortezomib is an efficacious apoptotic agent in many tumor cells. This paper shows that bortezomib induced apoptosis in human hepatoma HepG2 cells associated with many modifications in the expression of survival or death factors. Although bortezomib increased the level of the protective factors HSP70 and HSP27, the effects of the drug that favour cell death were predominant. These events include accumulation of c-Jun, phospho-c-Jun and p53; increase in FasL level with activation of caspase-8; changes related to members of Bcl-2 family with increase in the level of pro-apoptotic members and decrease in that of anti-apoptotic ones; dissipation of mitochondrial potenti…

Cancer ResearchProgrammed cell deathFas Ligand ProteinProto-Oncogene Proteins c-junClinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsApoptosisCaspase 8Cell LineBortezomibHsp27Cell Line TumormedicineHumansMitogen-Activated Protein Kinase 8Protease InhibitorsAP1Heat-Shock ProteinsPharmacologyCaspase 8Membrane GlycoproteinsbiologyJNK.Bortezomibc-JunLiver NeoplasmsBiochemistry (medical)c-junhepatomaCell BiologyapoptosiBoronic AcidsMitochondriaCell biologyTranscription Factor AP-1AP-1 transcription factorLiverProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesPyrazinesTumor Necrosis Factorsbiology.proteinCancer researchProteasome inhibitorSignal Transductionmedicine.drugApoptosis
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Apoptosis induced by (E)-5-(2-bromovinyl)-2'-deoxyuridine in varicella zoster virus thymidine kinase-expressing cells is driven by activation of c-Ju…

2003

The molecular mode of cell killing by the antiviral drug (E)-5-(2-bromovinyl-2'-deoxyuridine (BVDU) was studied in Chinese hamster ovary (CHO) cells stably transfected with the thymidine kinase gene (tk) of varicella zoster virus (CHO-VZVtk). The colony-forming ability of the cells was reduced to <1% at a concentration of approximately 1 microM BVDU, whereas for nontransfected cells or cells transfected with tk gene of herpes simplex virus type 1 (CHO-HSVtk), a 1000-fold higher dose was required to achieve the same response. BVDU inhibited thymidylate synthase in CHO-VZVtk but not in CHO-HSVtk and control cells. On the other hand, the drug was incorporated into DNA of VZVtk- and HSVtk-expre…

Herpesvirus 3 HumanFas Ligand ProteinFas-Associated Death Domain ProteinApoptosisCHO CellsBiologyTransfectionAntiviral AgentsThymidine KinaseFas ligandchemistry.chemical_compoundNecrosisCricetinaeCytotoxic T cellAnimalsSimplexvirusAdaptor Proteins Signal TransducingPharmacologyCaspase 8GenomeMembrane GlycoproteinsChinese hamster ovary cellCell CycleJNK Mitogen-Activated Protein KinasesTransfectionDNAThymidylate SynthaseMolecular biologyCaspase 9Transcription Factor AP-1Cell killingchemistryBromodeoxyuridineApoptosisThymidine kinaseCaspasesMolecular MedicineMitogen-Activated Protein KinasesCarrier ProteinsBromodeoxyuridineMolecular pharmacology
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Evidence for an instructive role of apoptosis during the metamorphosis of Hydractinia echinata (Hydrozoa)

2011

Apoptosis is a highly conserved mechanism of cell deletion that destroys redundant, dysfunctional, damaged, and diseased cells. Furthermore, apoptotic cell death is essential during the development of multicellular organisms. However, there are only a few examples where the occurrence of apoptosis has been shown to be a direct prerequisite for developmental processes. As described previously by our group, the degradation of larval tissue during the first half of the metamorphosis of Hydractinia echinata involves extensive cell death. A large number of cells are removed, and we observed several cellular features of apoptotic cell death in the dying tissue, e.g., nucleosomal DNA fragmentation…

Programmed cell deathmedia_common.quotation_subjectMolecular Sequence DataCellApoptosisContext (language use)Gene Expression Regulation EnzymologicHydractinia echinatamedicineAnimalsAmino Acid SequenceMetamorphosisConserved SequencePhylogenyCaspasemedia_commonbiologyGene Expression ProfilingMetamorphosis Biologicalbiology.organism_classificationCell biologyHydrozoamedicine.anatomical_structureApoptosisCaspasesGene Knockdown Techniquesbiology.proteinDNA fragmentationAnimal Science and ZoologySequence AlignmentZoology
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A lytic mechanism based on soluble phospholypases A2 (sPLA2) and b-galactoside specific lectins is exerted by Ciona intestinalis (ascidian) unilocula…

2011

Abstract Hemocytes from the ascidian Ciona intestinalis exert in vitro Ca 2+ -dependent cytotoxic activity toward mammalian erythrocytes and K562 cells. To examine the lytic mechanism, hemocyte populations were separated (B1–B6 bands) through a Percoll discontinuous density gradient, the hemocyte cytotoxic activity (HCA) and the lytic activity of the hemocyte lysate supernatant (HLS) were assayed. In addition the separated hemocytes were cultured and the cell-free culture medium (CFM) assayed after 3 h culture. Results support that unilocular refractile hemocytes (URGs), enriched in B5, are cytotoxic. The B5-HLS contains lysins and the activity of B5-CFM shows that lysins can be released in…

HemocytesPhospholipase A2 Inhibitorsmedicine.medical_treatmentLysinDibucaineSettore BIO/05 - ZoologiaAquatic ScienceBiologyFucoseCell membranechemistry.chemical_compoundmedicineEnvironmental ChemistryAnimalsHumansCiona intestinalisLectins C-TypeEnzyme InhibitorsProteaseErythrocyte MembraneGeneral Medicinebiology.organism_classificationCytotoxicity Tests Immunologicbeta-GalactosidaseGalactosideCiona intestinalisPhospholipases A2medicine.anatomical_structurechemistryBiochemistryLytic cycleInvertebrate immunity Ciona intestinalis Hemocyte Cytotoxicity Soluble phospholipase A2 Rabbit erythrocyte K562QuinacrineCaspasesImmunologyMicroscopy Electron ScanningRabbitsK562 CellsPercoll
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Induction of apoptosis by arachidonic acid in human retinoblastoma Y79 cells: involvement of oxidative stress

2000

Arachidonic acid administration caused apoptosis in Y79 cells, as shown by typical morphological changes, phosphatidylserine externalization, chromatin condensation, processing and activation of caspase-3 and cleavage of the endogenous caspase substrate poly-(ADP-ribose)-polymerase. Arachidonic acid also caused lamin B cleavage, suggesting caspase-6 activation. Arachidonic acid treatment was accompanied by increased formation of the lipid peroxidation end products malondialdehyde and 4-hydroxy-2-nonenal, lowering in reduced glutathione content and in mitochondrial membrane potential. Inhibiting glutathione synthesis sensitized Y79 cells to apoptosis-inducing stimuli, whilst replenishing red…

Cell SurvivalBlotting WesternApoptosisCell Countmedicine.disease_causeMembrane PotentialsLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundPhospholipase A2medicineTumor Cells Culturedarachidonic acidHumansCYP2C8biologyDose-Response Relationship DrugRetinoblastomaGlutathioneTrypan BlueMalondialdehydeFlow CytometryGlutathioneSensory SystemsCell biologyMitochondriaOphthalmologyOxidative StressBiochemistrychemistryMitochondrial permeability transition poreCaspasesbiology.proteinArachidonic acidColorimetryPoly(ADP-ribose) PolymerasesOxidative stress
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pp32/PHAPI determines the apoptosis response of non-small-cell lung cancer

2007

During malignant transformation, cancer cells have to evade cell-intrinsic tumor suppressor mechanisms including apoptosis, thus acquiring a phenotype that is relatively resistant to clinically applied anticancer therapies. Molecular characterization of apoptotic signal transduction defects may help to identify prognostic markers and to develop novel therapeutic strategies. To this end we have undertaken functional analyses of drug-induced apoptosis in human non-small cell-lung cancer (NSCLC) cells. We found that primary drug resistance correlated with defects in apoptosome-dependent caspase activation in vitro. While cytochrome c-induced apoptosome formation was maintained, the subsequent …

Lung NeoplasmsTransplantation HeterologousAntineoplastic AgentsApoptosisMice SCIDBiologyMalignant transformationMiceProstate cancerIn vivoCarcinoma Non-Small-Cell LungmedicineAnimalsHumansLung cancerMolecular BiologyIntracellular Signaling Peptides and ProteinsNuclear ProteinsRNA-Binding ProteinsCancerCell Biologymedicine.diseaseCell biologyEnzyme ActivationApoptosisCaspasesCancer cellCancer researchSignal transductionNeoplasm TransplantationCell Death &amp; Differentiation
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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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The sea urchin embryo: a model to study Alzheimer's beta amyloid induced toxicity.

2009

Abstract Alzheimer’s disease (AD) is the most common form of dementia. The cause of AD is closely related to the accumulation of amyloid beta peptide in the neuritic plaques. The use of animal model systems represents a good strategy to elucidate the molecular mechanism behind the development of this pathology. Here we use the Paracentrotus lividus embryo to identify molecules and pathways that can be involved in the degenerative process. As a first step, we identified the presence of an antigen related to the human APP, called Pl APP. This antigen, after gastrula stage, is processed producing a polypeptide of about 10 kDa. By immunohistochemistry we localized the Pl APP antigen in some ser…

AmyloidAmyloid betaBiophysicsApoptosisBiochemistryNervous SystemParacentrotus lividusAlzheimer Diseasebiology.animalAnimalsHumansSenile plaquesAntigensMolecular BiologySea urchinCaspaseTUNEL assayAmyloid beta-Peptidesbiologybiology.organism_classificationPeptide FragmentsRecombinant ProteinsCell biologyBiochemistryApoptosisCaspasesModels Animalbiology.proteinParacentrotusParacentrotus lividusAmyloid-betaOligomers Fibrillar aggregatesApoptosisAnimal modelArchives of biochemistry and biophysics
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Genetic manipulation of longevity-related genes as a tool to regulate yeast life span and metabolite production during winemaking

2013

Abstract Background Yeast viability and vitality are essential for different industrial processes where the yeast Saccharomyces cerevisiae is used as a biotechnological tool. Therefore, the decline of yeast biological functions during aging may compromise their successful biotechnological use. Life span is controlled by a variety of molecular mechanisms, many of which are connected to stress tolerance and genomic stability, although the metabolic status of a cell has proven a main factor affecting its longevity. Acetic acid and ethanol accumulation shorten chronological life span (CLS), while glycerol extends it. Results Different age-related gene classes have been modified by deletion or o…

HST3GlycerolSaccharomyces cerevisiae ProteinsTranscription Genetic<it>HST3</it>Saccharomyces cerevisiaeLongevitylcsh:QR1-502SOD2BioengineeringApoptosisWinePUB1Saccharomyces cerevisiaeStressApplied Microbiology and Biotechnologylcsh:MicrobiologyHistone DeacetylasesStress granuleSirtuin 2<it>PUB1</it>Gene expressionChronological agingSirtuinsNADH NADPH OxidoreductasesRNA MessengerEthanol metabolismSilent Information Regulator Proteins Saccharomyces cerevisiaeAcetic AcidbiologyEthanolSuperoxide DismutaseResearchRNA-Binding Proteinsbiology.organism_classificationYeastYeastBiochemistryCaspasesFermentationMutationFermentationHistone deacetylaseGene DeletionBiotechnologyMicrobial Cell Factories
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Oxysterol mixture in hypercholesterolemia-relevant proportion causes oxidative stress-dependent eryptosis.

2014

Background/Aims: Oxysterol activity on the erythrocyte (RBC) programmed cell death (eryptosis) had not been studied yet. Effects of an oxysterol mixture in hyper-cholesterolemic-relevant proportion, and of individual compounds, were investigated on RBCs from healthy humans. Methods: Membrane phosphatidylserine (PS) externalization, calcium entry, ROS production, amino-phospholipid translocase (APLT) activity were evaluated by cytofluorimetric assays, cell volume from forward scatter. Prostaglandin PGE2 was measured by ELISA; GSH-adducts and lipoperoxides by spectrophotometry. Involvement of protein kinase C and caspase was investigated by inhibitors staurosporin, calphostin C, and Z-DEVD-FM…

ErythrocytesPhysiologyEryptosisApoptosisPharmacologylcsh:PhysiologyAntioxidantschemistry.chemical_compoundPhospholipid scramblingSettore BIO/10 - Biochimicapolycyclic compoundslcsh:QD415-436PhosphatidylserineKetocholesterolsProtein Kinase Clcsh:QP1-981OxysterolsPhosphatidylserineErythrocyteCalphostin CBiochemistryCaspaseslipids (amino acids peptides and proteins)AntioxidantReactive Oxygen SpecieHumanProgrammed cell deathOxysterolHypercholesterolemiachemistry.chemical_elementPhosphatidylserinesCalciumCalcium ChannelDinoprostonelcsh:BiochemistryOxysterolLipid oxidationHumansCalphostinHypercholesterolemia Human red blood cell Oxysterols Eryptosis Oxidative stressKetocholesterolApoptosiOxidative StreCaspaseOxidative StresschemistryCalciumCalcium ChannelsReactive Oxygen SpeciesEryptosiHuman red blood cellCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
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