Search results for "CASP"

showing 10 items of 470 documents

2014

Background In models of COPD, environmental stressors induce innate immune responses, inflammasome activation and inflammation. However, the interaction between these responses and their role in driving pulmonary inflammation in stable COPD is unknown. Objectives To investigate the activation of innate immunity and inflammasome pathways in the bronchial mucosa and bronchoalveolar lavage (BAL) of patients with stable COPD of different severity and control healthy smokers and non-smokers. Methods Innate immune mediators (interleukin (IL)-6, IL-7, IL-10, IL-27, IL-37, thymic stromal lymphopoietin (TSLP), interferon γ and their receptors, STAT1 and pSTAT1) and inflammasome components (NLRP3, NA…

Pulmonary and Respiratory MedicineCOPDThymic stromal lymphopoietinInnate immune systemmedicine.diagnostic_testbiologybusiness.industryCaspase 1NALP3InflammationInflammasomemedicine.diseaserespiratory tract diseases3. Good healthBronchoalveolar lavageImmunologymedicinebiology.proteinmedicine.symptombusinessmedicine.drugThorax
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CD40 ligation protects bronchial epithelium against oxidant-induced caspase-independent cell death.

2006

KEYWORDS CLASSIFICATION: 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide;Antigens,CD40;Apoptosis;Bronchi;cytology;Caspases;Cell Cycle;Cell Death;Cell Line,Transformed;Cell Survival;Cell Transformation,Viral;Cytoprotection;drug effects;Epithelial Cells;Humans;Italy;mechanisms of carcinogenesis;metabolism;Oxidants;pharmacology;physiology;Research;Simian virus 40;toxicity;Transcription Factor AP-1. CD40 and its ligand regulate pleiotropic biological responses, including cell proliferation, differentiation, and apoptosis. In many inflammatory lung diseases, tissue damage by environmental or endogenous oxidants plays a major role in disease pathogenesis. As the epithelial barrier is a major t…

Pulmonary and Respiratory MedicineNF-BProgrammed cell deathCell SurvivalClinical Biochemistry78-Dihydro-78-dihydroxybenzo(a)pyrene 910-oxideApoptosisBronchiSimian virus 40Inhibitor of apoptosisAntigens CD40CD40HumansCD40 AntigensMolecular BiologyMitosisCaspaseActivator protein–1Cell Line Transformedoxidant stressbiologyCell DeathCell growthCell CycleEpithelial CellsCell BiologyCell cycleCell Transformation ViralOxidantsapoptosiCell biologyTranscription Factor AP-1activator protein–1ApoptosisCytoprotectionCaspasesbiology.proteinNF- BApoptosis-inducing factorOxidant stress
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Rho protein inactivation induced apoptosis of cultured human endothelial cells.

2002

Small GTP-binding Rho GTPases regulate important signaling pathways in endothelial cells, but little is known about their role in endothelial cell apoptosis. Clostridial cytotoxins specifically inactivate GTPases by glucosylation [ Clostridium difficile toxin B-10463 (TcdB-10463), C. difficile toxin B-1470 (TcdB-1470)] or ADP ribosylation ( C. botulinum C3 toxin). Exposure of human umbilical cord vein endothelial cells (HUVEC) to TcdB-10463, which inhibits RhoA/Rac1/Cdc42, or to C3 toxin, which inhibits RhoA, -B, -C, resulted in apoptosis, whereas inactivation of Rac1/Cdc42 with TcdB-1470 was without effect, suggesting that Rho inhibition was responsible for endothelial apoptosis. Disruptio…

Pulmonary and Respiratory Medicinerac1 GTP-Binding Proteinrho GTP-Binding ProteinsProgrammed cell deathUmbilical VeinsEndotheliumPhysiologyBacterial ToxinsCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBcl-2-associated X proteinBacterial ProteinsPhysiology (medical)Proto-Oncogene ProteinsmedicineCyclic AMPIn Situ Nick-End LabelingHumanscdc42 GTP-Binding ProteinCells Culturedbcl-2-Associated X ProteinAdenosine Diphosphate RibosebiologyCaspase 3Intracellular Signaling Peptides and ProteinsCell BiologyCaspase 9Cell biologyNeoplasm ProteinsEndothelial stem cellmedicine.anatomical_structureCdc42 GTP-Binding ProteinProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisCaspasesbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinEndothelium VascularSignal transductionCarrier ProteinsrhoA GTP-Binding ProteinBH3 Interacting Domain Death Agonist ProteinSignal TransductionAmerican journal of physiology. Lung cellular and molecular physiology
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Prediction of new inorganic molecules with quantum chemical methods

2006

Quantum chemistry can today be employed to invent new molecules and explore unknown molecular bonding. An overview of novel species containing metals bound to polynitrogen clusters is presented. The prediction of metal polyhydrides is discussed. Finally, some species containing gold that behaves as a halogen are described, together with recent advances in actinide chemistry and exploration of the nature of the actinide–actinide chemical bonding.

Quantum chemicalActinide chemistryCASPT2ChemistryActinideQuantum chemistryActinidesMetalChemical bondChemical physicsvisual_artddc:540Halogenvisual_art.visual_art_mediumMoleculeMetal-polynitrogen clustersMetal polyhydridesGoldPhysical and Theoretical Chemistry
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A radiosensitizing effect of artesunate in glioblastoma cells is associated with a diminished expression of the inhibitor of apoptosis protein surviv…

2011

Abstract Background and purpose Novel strategies to overcome an irradiation resistant phenotype may help to increase therapeutic efficacy in glioblastoma multiforme. The present study aimed to elucidate radiation sensitizing properties of artesunate, a semi synthetic derivate of artemisinin and to assess factors involved in this effect. Materials and methods LN229 and U87MG cells were treated with various concentrations of artesunate and radiation response was determined by a colony forming assay. Cell numbers, apoptosis induction, cell cycle distribution, and DNA repair following combined modality treatment were monitored by MTT-, caspase 3/7 assay, cytofluorometry, and γ-H2AX foci formati…

Radiation-Sensitizing AgentsDNA RepairCell SurvivalSurvivinArtesunateDown-RegulationCaspase 3ApoptosisInhibitor of apoptosisInhibitor of Apoptosis Proteinschemistry.chemical_compoundCell Line TumorSurvivinHumansRadiology Nuclear Medicine and imagingClonogenic assayDose-Response Relationship DrugBrain NeoplasmsCell CycleHematologyCell cycleArtemisininsXIAPNeoplasm ProteinsOncologychemistryArtesunateApoptosisCancer researchGlioblastomaRadiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
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Hamster Bcl-2 Protein Is Cleaved in Vitro and in Cells by Caspase-9 and Caspase-3

2001

Full-length cDNA of hamster bcl-2 (771 nt) was cloned by RT-PCR and inserted into pGEX-4T-1 to produce the recombinant hamster Bcl-2 protein. The purified recombinant Bcl-2 protein (26.4 kDa) was used as a substrate for the active human caspase-3 and caspase-9 in vitro. It is shown here that Bcl-2 is efficiently cleaved by caspase-3 to a 23 kDa fragment. Although not possessing a putative caspase-9 cleavage site in its sequence, hamster Bcl-2 was also cleaved by caspase-9 into exactly the same 23 kDa cleavage product, indicating that cleavage occurred at the same site. Caspase-3- and caspase-9-mediated cleavage of Bcl-2 was efficiently blocked by caspase-3 (zDEVD) and caspase-9 (zLEHD) inhi…

Recombinant Fusion ProteinsBlotting WesternBiophysicsHamsterCaspase 3CHO CellsCysteine Proteinase InhibitorsCleavage (embryo)Biochemistrylaw.inventionlawCricetinaeComplementary DNAAnimalsHumansMolecular BiologyCaspaseGlutathione TransferaseCleavage stimulation factorbiologyCaspase 3Chinese hamster ovary cellThrombinCell BiologyCaspase InhibitorsMolecular biologyCaspase 9Proto-Oncogene Proteins c-bcl-2Caspasesbiology.proteinRecombinant DNAOligopeptidesBiochemical and Biophysical Research Communications
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SAHA/TRAIL combination induces detachment and anoikis of MDA-MB231 and MCF-7 breast cancer cells

2012

Abstract SAHA, an inhibitor of histone deacetylase activity, has been shown to sensitize tumor cells to apoptosis induced by TRAIL, a member of TNF-family. In this paper we investigated the effect of SAHA/TRAIL combination in two breast cancer cell lines, the ERα−positive MCF-7 and the ERα−negative MDA-MB231. Treatment of MDA-MB231 and MCF-7 cells with SAHA in combination with TRAIL caused detachment of cells followed by anoikis, a form of apoptosis which occurs after cell detachment, while treatment with SAHA or TRAIL alone did not produce these effects. The effects were more evident in MDA-MB231 cells, which were chosen for ascertaining the mechanism of SAHA/TRAIL action. Our results show…

Recombinant Fusion ProteinsCellCASP8 and FADD-Like Apoptosis Regulating ProteinAntineoplastic AgentsBreast NeoplasmsHydroxamic AcidsCleavage (embryo)BiochemistryTNF-Related Apoptosis-Inducing LigandCell Line TumorProto-Oncogene ProteinsSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsCell AdhesionmedicineSAHA TRAIL Anoikis EGFR FAK BimELHumansAnoikisskin and connective tissue diseasesMda mb231VorinostatBcl-2-Like Protein 11ChemistryMembrane ProteinsGeneral MedicineAnoikisErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureMCF-7ApoptosisCaspasesFocal Adhesion Kinase 1ImmunologyCancer researchPhosphorylationFemaleHistone deacetylase activityApoptosis Regulatory ProteinsSignal Transduction
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T47-D Cells and Type V Collagen: A Model for the Study of Apoptotic Gene Expression by Breast Cancer Cells

2003

We have previously reported that type V collagen is a poorly adhesive, anti-proliferative and motility-inhibitory substrate for the 8701-BC breast cancer cell line, which also triggers DNA fragmentation and impairs survival of the same cell line. In the present work we have extended to other breast cancer cell lines (T47-D, MDA-MB231, Hs578T) our investigation of type V collagen influence on the DNA status and cell survival, also examining whether adhesion and growth of cells on this collagen substrate could exert some effect on the expression level of selected apoptosis-related genes. We report here that, among the cell lines tested, only T47-D is responsive to the death-promoting influenc…

Regulation of gene expressionMammary tumorCell typebiologyCell divisionClinical BiochemistryApoptosisBreast NeoplasmsBiochemistryCell biologyGene Expression RegulationCell cultureCell Line TumorCell Adhesionbiology.proteinHumansDNA fragmentationskin and connective tissue diseasesCell adhesionCollagen Type VMolecular BiologyCell DivisionCaspaseBiological Chemistry
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Les IAP au cœur de la signalisation NF-κB

2012

The function of IAP has long been limited to an inhibition of apoptosis through their capacity to bind some caspases. Since the expression of these proteins is altered in some tumor samples, IAPs are targets for anticancer therapy and many small molecules have been designed for their capacity to inhibit IAP-caspase interaction. Unexpectedly, these molecules appeared to significantly affect NF-κB activation. In this review, we will discuss the central role of cIAP1, cIAP2 and XIAP in the regulation of NF-κB activating signaling pathways.

Regulation of gene expressionbiologyGeneral MedicineTransforming growth factor betaNFKB1General Biochemistry Genetics and Molecular BiologyCell biologyXIAPbody regionsApoptosisImmunologybiology.proteinSignal transductionReceptorCaspasemédecine/sciences
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A novel copper compound, CuNV110, induces apoptosis in tumor cells by dissociation of the Hsp60- pro-caspase 3 complex

2015

The biological activity of CuNV1110, a novel copper chemical compound, has been recently studied on cancer cells and it has been showed that it reduces the cell viability, in a dose and time dependent manner, and induces cell apoptosis. In this study we evaluated the possible mechanisms by which CuNV1110 induces cell apoptosis. In particular we looked at its effects on Hsp60 levels and caspase 3 activation. We used an in vitro model of a pulmonary mucoepidermoid carcinoma (NCI-H292 cells). We found that CuNV1110 reduces the cell viability and induces cell apoptosis in a dose/time dependent manner. Then, we found that Hsp60 levels decrease with the increasing concentrations of CuNV110; by co…

Respiratory cells; pulmonary cancer; Hsp60; caspase 3; apoptosis.Respiratory cells pulmonary cancer Hsp60 caspase 3 apoptosis
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