Search results for "Caspase Inhibitor"

showing 10 items of 26 documents

Smac induces cytochrome c release and apoptosis independently from Bax/Bcl-xL in a strictly caspase-3-dependent manner in human carcinoma cells

2004

The mitochondrial apoptosis pathway mediates cell death through the release of various pro-apoptotic factors including cytochrome c and Smac, the second mitochondrial activator of caspases, into the cytosol. Smac was shown previously to inhibit IAP proteins and to facilitate initiation of the caspase cascade upon cytochrome c release. To investigate Smac function during apoptosis and to explore Smac as an experimental cancer therapeutic, we constructed an expression system based on a single adenoviral vector containing Smac under control of the Tet-off system supplied in cis. Conditional expression of Smac induced apoptosis in human HCT116 and DU145 carcinoma cells regardless of the loss of…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsBcl-xLCaspase 3Cysteine Proteinase InhibitorsAdenoviridaeMitochondrial ProteinsBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedGeneticsHumansMolecular BiologyCaspasebcl-2-Associated X ProteinCaspase-9biologyCaspase 3Cytochrome cCarcinomaIntracellular Signaling Peptides and ProteinsCytochromes cCaspase InhibitorsCaspase 9Cell biologyEnzyme ActivationProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesMutationbiology.proteinCancer researchbiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsCarrier ProteinsOligopeptidesProtein Processing Post-TranslationalOncogene
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Dinitrosyl-iron triggers apoptosis in Jurkat cells despite overexpression of Bcl-2

2004

Cells expressing the cytokine-inducible NO synthase are known to trigger apoptosis in neighboring cells. Paramagnetic dinitrosyl nonheme iron complexes (DNIC) were found in tumor tissue about 40 years ago; however, the role of these NO(+)-bearing species is not completely understood. In the human Jurkat leukemia cell line, the application of the model complex DNIC-thiosulfate (50-200 microM) induced apoptosis (defined by phosphatidylserine externalization) in a concentration- and time-dependent manner. In Jurkat cells, the pan-caspase inhibitor, zVADfmk (50 microM), and/or stable transfection of antiapoptotic protein, Bcl-2, was unable to afford protection against DNIC-induced apoptosis. Th…

IronNitrosationCellApoptosisBiochemistryJurkat cellsMetal ChelatorNitric oxideJurkat Cellschemistry.chemical_compoundPhysiology (medical)medicineExtracellularPiHumansElectron Spin Resonance SpectroscopyGlutathioneCaspase InhibitorsCell biologymedicine.anatomical_structureGene Expression RegulationProto-Oncogene Proteins c-bcl-2chemistryApoptosisCaspasesNitrogen OxidesFree Radical Biology and Medicine
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Caspase-mediated apoptosis in sponges: cloning and function of the phylogenetic oldest apoptotic proteases from Metazoa

2003

AbstractSponges (phylum Porifera) represent the phylogenetically oldest metazoan phylum. These animals have complex cell adhesion and powerful immune systems which allow the formation of a distinct body plan. Consequently, an apoptotic machinery has to be predicted that allows sponges to eliminate unwanted cells accumulating during development. With the marine sponge Geodia cydonium, it is shown that allografts of these animals undergo apoptosis as demonstrated by apoptotic DNA fragmentation. Extracts from allografts contain an enzymic activity characteristic for caspases; as substrate to determine the cleavage activity, Ac-DEVD-AMC was applied. cDNAs encoding predicted caspase-3-related pr…

Molecular Sequence DataApoptosisCaspase 3SpongeCoumarinsEndopeptidasesAnimalsInvertebrateAmino Acid SequenceCloning MolecularEnzyme InhibitorsMolecular BiologyPhylogenyCaspasebiologyCaspase 3Cell adhesion moleculeAlternative splicingApoptotic DNA fragmentationPotential proapoptotic molecule DD2Cell BiologyBcl-2 homologous proteinbiology.organism_classificationSuberites domunculaCaspaseCaspase InhibitorsPoriferaCell biologyIsoenzymesSuberites domunculaSpongeApoptosisCaspasesbiology.proteinOligopeptidesSequence AlignmentBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Cell proliferation and DNA breaks are involved in ultraviolet light-induced apoptosis in nucleotide excision repair-deficient Chinese hamster cells.

2002

UV light targets both membrane receptors and nuclear DNA, thus evoking signals triggering apoptosis. Although receptor-mediated apoptosis has been extensively investigated, the role of DNA damage in apoptosis is less clear. To analyze the importance of DNA damage induced by UV-C light in apoptosis, we compared nucleotide excision repair (NER)-deficient Chinese hamster ovary cells (lines 27-1 and 43-3B mutated for the repair genes ERCC3 and ERCC1, respectively) with the corresponding DNA repair-proficient fibroblasts (CHO-9 and ERCC1 complemented 43-3B cells). NER-deficient cells were hypersensitive as to the induction of apoptosis, indicating that apoptosis induced by UV-C light is due to u…

DNA RepairTranscription GeneticDNA repairDNA damageCell SurvivalUltraviolet RaysApoptosisCHO CellsBiologyCysteine Proteinase InhibitorsRadiation ToleranceArticleMiceCricetinaeUltraviolet lightAnimalsMolecular BiologyChromosome AberrationsIntrinsic apoptosisCell CycleDNA replicationCell BiologyFibroblastsMolecular biologyCaspase InhibitorsChromatinCell biologyKineticsUVB-induced apoptosisProto-Oncogene Proteins c-bcl-2ApoptosisMutationTumor Suppressor Protein p53Cell DivisionNucleotide excision repairDNA DamageMolecular biology of the cell
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Aβ Oligomers and Fibrillar Aggregates Induce Different Apoptotic Pathways in LAN5 Neuroblastoma Cell Cultures

2009

Fibril deposit formation of amyloid beta-protein (Abeta) in the brain is a hallmark of Alzheimer's disease (AD). Increasing evidence suggests that toxicity is linked to diffusible Abeta oligomers, which have been found in soluble brain extracts of AD patients, rather than to insoluble fibers. Here we report a study of the toxicity of two distinct forms of recombinant Abeta small oligomers and fibrillar aggregates to simulate the action of diffusible Abeta oligomers and amyloid plaques on neuronal cells. Different techniques, including dynamic light scattering, fluorescence, and scanning electron microscopy, have been used to characterize the two forms of Abeta. Under similar conditions and …

Time FactorsAmyloidCell SurvivalBiophysicsApoptosisBiologyFibrilCaspase 8Substrate SpecificityNeuroblastomaCytosolCell Line TumormedicineHumansEnzyme InhibitorsProtein Structure QuaternaryCaspase-9Amyloid beta-PeptidesDose-Response Relationship DrugProteinCytochrome cNeurodegenerationCytochromes cHydrogen-Ion Concentrationmedicine.diseaseCaspase InhibitorsPeptide FragmentsCell biologyProtein TransportCytosolApoptosisMicroscopy Electron Scanningbiology.proteinProtein MultimerizationProtein BindingSignal TransductionBiophysical Journal
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Berberine inhibits cell growth and mediates caspase-independent cell death in human pancreatic cancer cells.

2010

Pancreatic cancer is one of the most aggressive human malignancies with an increasing incidence worldwide. In addition to the poor survival rates, combinations using gemcitabine as a backbone have failed to show any benefit beyond monotherapy. These facts underscore an urgent need for novel therapeutic options and motivated us to study the effect of berberine on pancreatic cancer cells. Here, we undertook an mRNA-based gene expression profiling study in order to get deeper insight into the molecular targets mediating the growth inhibitory effects of berberine on pancreatic cancer cells compared to normal ones. Twenty-four hours after treatment, berberine showed preferential selectivity towa…

Programmed cell deathmedicine.medical_specialtyBerberineDNA damagePharmaceutical ScienceApoptosisAnalytical Chemistrychemistry.chemical_compoundBerberinePancreatic cancerInternal medicineCell Line TumorDrug DiscoverymedicineHumansRNA MessengerCell ProliferationOligonucleotide Array Sequence AnalysisPharmacologybiologyCell growthTopoisomeraseGene Expression ProfilingOrganic ChemistryCancermedicine.diseaseAntineoplastic Agents PhytogenicCaspase InhibitorsImmunohistochemistryEnzyme ActivationPancreatic NeoplasmsEndocrinologyComplementary and alternative medicinechemistryApoptosisCaspasesbiology.proteinCancer researchMolecular MedicineSignal TransductionPlanta medica
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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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Effects of caspase inhibitors (z-VAD-fmk, z-VDVAD-fmk) on Nile Red fluorescence pattern in 7-ketocholesterol-treated cells: Investigation by flow cyt…

2007

Background: The 7-ketocholesterol (7KC)-induced cell death has some characteristics of apoptosis and is associated with polar lipid accumulation. So, we investigated the effects of the broad-spectrum caspase inhibitor z-VAD-fmk and of the caspase-2 inhibitor z-VDVAD-fmk on lipid profile evaluated by staining with Nile Red (NR). Methods: The 7KC-treated human monocytic U937 cells were cultured in the absence or in the presence of the caspase inhibitors z-VAD-fmk or z-VDVAD-fmk. When staining with NR is performed, neutral and polar lipids have yellow and orange/red emission, respectively, and fluorescence was then analyzed by flow cytometry (FCM) and by confocal laser scanning microscopy (CLS…

HistologyConfocalCaspase 2FluorescencePathology and Forensic Medicinelaw.inventionFlow cytometryAmino Acid Chloromethyl Ketones03 medical and health scienceschemistry.chemical_compound0302 clinical medicineConfocal microscopylawOxazinesmedicineImage Processing Computer-AssistedHumans[ SDV.IB ] Life Sciences [q-bio]/BioengineeringEnzyme InhibitorsKetocholesterols030304 developmental biology[SDV.IB] Life Sciences [q-bio]/BioengineeringCell Nucleus0303 health sciencesMicroscopyMicroscopy Confocalbiologymedicine.diagnostic_testNile redLipid metabolismCell BiologyU937 CellsFlow CytometryLipid MetabolismFluorescenceMolecular biologyCaspase Inhibitors3. Good healthStainingchemistry030220 oncology & carcinogenesisbiology.protein[SDV.IB]Life Sciences [q-bio]/Bioengineeringbiological phenomena cell phenomena and immunityFactor Analysis Statistical
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Spontaneous and Fas-induced apoptosis of low-grade MDS erythroid precursors involves the endoplasmic reticulum

2008

Spontaneous apoptosis of bone marrow erythroid precursors accounts for the anemia that characterizes most low-grade myelodysplastic syndromes (MDS). We have shown that death of these precursors involved the Fas-dependent activation of caspase-8. To explore the pathway leading from caspase-8 activation to apoptosis, we transduced MDS bone marrow CD34(+) cells with a lentivirus encoding wild-type (WT) or endoplasmic reticulum (ER)-targeted Bcl-2 protein before inducing their erythroid differentiation. Both WT-Bcl-2 and ER-targeted Bcl-2 prevented spontaneous and Fas-dependent apoptosis in MDS erythroid precursors. ER-targeted Bcl-2 inhibited mitochondrial membrane depolarization and cytochrom…

Cancer ResearchProgrammed cell deathApoptosis[SDV.BC]Life Sciences [q-bio]/Cellular BiologyMitochondrionEndoplasmic Reticulum03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineHumansfas ReceptorErythropoietinComputingMilieux_MISCELLANEOUS030304 developmental biologyErythroid Precursor Cells0303 health sciencesbiologyCytochrome cEndoplasmic reticulumMembrane ProteinsAnemiaHematologyCaspase InhibitorsMitochondria3. Good healthCell biologyRed blood cellmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyErythropoietinApoptosisMyelodysplastic Syndromes030220 oncology & carcinogenesisCancer researchbiology.protein[SDV.IMM]Life Sciences [q-bio]/ImmunologyCalciumBone marrowmedicine.drug
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Ultraviolet light-induced DNA damage triggers apoptosis in nucleotide excision repair-deficient cells via Bcl-2 decline and caspase-3/-8 activation.

2001

Ultraviolet (UV) light is a potent mutagenic and genotoxic agent. Whereas DNA damage induced by UV light is known to be responsible for UV-induced genotoxicity, its role in triggering apoptosis is still unclear. We addressed this issue by comparing nucleotide excision repair (NER) deficient 27-1 and 43-3B Chinese hamster (CHO) cells with the corresponding wild-type and ERCC-1 complemented cells. It is shown that NER deficient cells are dramatically hypersensitive to UV-C induced apoptosis, indicating that DNA damage is the major stimulus for the apoptotic response. Apoptosis triggered by UV-C induced DNA damage is related to caspase- and proteosome-dependent degradation of Bcl-2 protein. Th…

Cancer ResearchDNA RepairDNA repairDNA damageUltraviolet RaysPoly ADP ribose polymeraseFas-Associated Death Domain ProteinApoptosisCHO CellsBiologyCysteine Proteinase InhibitorsCaspase 8TransfectionFas ligandMembrane PotentialsCricetinaeGeneticsUltraviolet lightAnimalsRNA MessengerMolecular BiologyAdaptor Proteins Signal TransducingCaspase 8Caspase 3Fas receptorMolecular biologyCaspase InhibitorsCaspase 9MitochondriaEnzyme ActivationProto-Oncogene Proteins c-bcl-2CaspasesPoly(ADP-ribose) PolymerasesCarrier ProteinsNucleotide excision repairDNA DamageOncogene
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