Search results for "Programmed cell death"

showing 10 items of 609 documents

Sarcophytolide: a new neuroprotective compound from the soft coral Sarcophyton glaucum

1998

Abstract Bioactivity-guided fractionation of an alcohol extract of the soft coral Sarcophyton glaucum collected from the intertidal areas and the fringing coral reefs near Hurghada, Red Sea, Egypt resulted in the isolation of a new lactone cembrane diterpene, sarcophytolide. The structure of this compound was deduced from its spectroscopic data and by comparison of the spectral data with those of known closely related cembrane-type compounds. In antimicrobial assays, the isolated compound exhibited a good activity towards Staphylococcus aureus, Pseudomonas aeruginosa , and Saccharomyces cerevisiae. Sarcophytolide was found to display a strong cytoprotective effect against glutamate-induced …

Staphylococcus aureusProgrammed cell deathSecondary metaboliteToxicologyNeuroprotectionCnidariaMicechemistry.chemical_compoundmedicineAnimalsRats WistarGlutamate receptorNeurotoxicityBiological activitymedicine.diseaseMolecular biologyRatsNeuroprotective AgentsProto-Oncogene Proteins c-bcl-2chemistryBiochemistryNMDA receptorCalciumDiterpenesDiterpenemedicine.drugToxicology
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Tolerance without clonal expansion: self-antigen-expressing B cells program self-reactive T cells for future deletion.

2008

Abstract B cells have been shown in various animal models to induce immunological tolerance leading to reduced immune responses and protection from autoimmunity. We show that interaction of B cells with naive T cells results in T cell triggering accompanied by the expression of negative costimulatory molecules such as PD-1, CTLA-4, B and T lymphocyte attenuator, and CD5. Following interaction with B cells, T cells were not induced to proliferate, in a process that was dependent on their expression of PD-1 and CTLA-4, but not CD5. In contrast, the T cells became sensitive to Ag-induced cell death. Our results demonstrate that B cells participate in the homeostasis of the immune system by abl…

T-LymphocytesProgrammed Cell Death 1 ReceptorAutoimmunityAntigens CD/biosynthesisAntigens CD5/geneticsAutoantigensInterleukin 21MiceImmunology and AllergyCytotoxic T cellHomeostasisCTLA-4 AntigenIL-2 receptorAntigens Differentiation/biosynthesisB-LymphocytesAntigens CD/geneticsB-Lymphocytes/immunologyT-Lymphocytes/metabolismNatural killer T cellCell biologymedicine.anatomical_structureHomeostasis/immunology2723 Immunology and AllergyAntigens CD5/biosynthesisAntigens Differentiation/geneticsAntigens CD5/immunologyT cellImmunologyAntigens CD/immunologyClonal Deletion610 Medicine & healthchemical and pharmacologic phenomenaMice TransgenicBiologyAutoantigens/biosynthesisCD5 AntigensAutoimmunity/physiologyAutoantigens/immunologyAntigens CDmedicineAnimalsB-Lymphocytes/metabolismAntigen-presenting cellCell Proliferation2403 ImmunologyAntigens Differentiation/immunologyGene Expression Regulation/immunologyCD40Clonal Deletion/physiologyT-Lymphocytes/immunologyAntigens Differentiation10040 Clinic for NeurologyB-1 cellGene Expression Regulationbiology.protein
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Retinoic Acid Induces Apoptosis-Associated Neural Differentiation of a Murine Teratocarcinoma Cell Line

2002

Abstract: Incubation with all-trans retinoic acid (RA) induces PCC7-Mz1 embryonic carcinoma cells to cease proliferation and to develop into a tissue-like pattern of neuronal, astroglial, and fibroblast-like derivatives over a period of several days. Concomitant with the induction of differentiation by RA, a sizable fraction of the Mz1 stem cells detaches and dies, with the maximal level of cell death achieved after 10 h of RA treatment. This RA-induced cell death fulfills all criteria of apoptosis, including nuclear condensation, intranucleosomal DNA degradation, expression of cysteine aspases (caspases), and the formation of apoptotic bodies. Apoptosis could be suppressed by the pan-caspa…

TeratocarcinomaProgrammed cell deathCellular differentiationRetinoic acidApoptosisTretinoinBiochemistryMiceCellular and Molecular Neurosciencechemistry.chemical_compoundGAP-43 ProteinTumor Cells CulturedAnimalsProtein Kinase CProtein kinase CCaspaseNeuronsbiologyCell DifferentiationGenes bcl-2Cell biologyGene Expression RegulationchemistryBiochemistryCell cultureApoptosisPhorbolbiology.proteinJournal of Neurochemistry
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Melatonin induces transcriptional regulation of Bim by FoxO3a in HepG2 cells

2012

Background: Melatonin induces apoptosis in many different cancer cell lines, including hepatocellular carcinoma cells. However, the responsible pathways have not been clearly elucidated. A member of the forkhead transcription factors' family, FoxO3a, has been implicated in the expression of the proapoptotic protein Bim (a Bcl-2-interacting mediator of cell death). In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate whether melatonin treatment induces Bim through regulation by the transcription factor FoxO3a. Methods: Cytotoxicity of melatonin was compared in HepG2 hepatoblastoma cells and primary human hepatocytes. Proapoptotic Bim expression was analys…

Transcriptional ActivationCancer Researchmedicine.medical_specialtyProgrammed cell deathSmall interfering RNACarcinoma HepatocellularTranscription GeneticApoptosisFoxO3amelatoninBiologyGenetics & GenomicsMelatoninDownregulation and upregulationCell Line TumorProto-Oncogene ProteinsInternal medicinemedicineTranscriptional regulationHumansGene silencingBimPhosphorylationRNA Small InterferingPromoter Regions GeneticTranscription factorBinding SitesBcl-2-Like Protein 11Forkhead Box Protein O3Membrane ProteinsForkhead Transcription FactorsHep G2 Cellshepatocellular carcinomaCell biologyEndocrinologyOncologyHepatocytesRNA Interferencebiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsChromatin immunoprecipitationProtein Bindingmedicine.drugBritish Journal of Cancer
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Nerve growth factor and epidermal growth factor stimulate clusterin gene expression in PC12 cells

1999

Clusterin (apolipoprotein J) is an extracellular glycoprotein that might exert functions in development, cell death and lipid transport. Clusterin gene expression is elevated at sites of tissue remodelling, such as differentiation and apoptosis; however, the signals responsible for this regulation have not been identified. We use here the clusterin gene as a model system to examine expression in PC12 cells under the control of differentiation and proliferation signals produced by nerve growth factor (NGF) and by epidermal growth factor (EGF) respectively. NGF induced clusterin mRNA, which preceded neurite outgrowth typical of neuronal differentiation. EGF also activated the clusterin mRNA, …

Transcriptional ActivationProgrammed cell deathNeuriteMolecular Sequence DataResponse ElementsTransfectionBinding CompetitivePC12 CellsBiochemistryEpidermal growth factorConsensus SequenceNeuritesAnimalsNerve Growth FactorsRNA MessengerCloning MolecularPromoter Regions GeneticMolecular BiologyGlycoproteinsSequence DeletionNeuronsRegulation of gene expressionMessenger RNABase SequenceEpidermal Growth FactorClusterinbiologyKinaseCell DifferentiationDNACell BiologyMolecular biologyeye diseasesRatsTranscription Factor AP-1ClusterinNerve growth factorbiology.proteinsense organsCell DivisionMolecular ChaperonesSignal TransductionResearch ArticleBiochemical Journal
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Heterocycle-containing retinoids. Discovery of a novel isoxazole arotinoid possessing potent apoptotic activity in multidrug and drug-induced apoptos…

2001

In a search for retinoic acid (RA) receptor ligands endowed with potent apoptotic activity, a series of novel arotinoids were prepared. Because the stereochemistry of the C9-alkenyl portion of natural 9-cis-RA and the olefinic moiety of the previously synthesized isoxazole retinoid 4 seems to have particular importance for their apoptotic activity, novel retinoid analogues with a restricted or, vice versa, a larger flexibility in this region were designed and prepared. The new compounds were evaluated in vitro for their ability to activate natural retinoid receptors and for their differentiation-inducing activity. Cytotoxic and apoptotic activities were, in addition, evaluated. In general, …

Transcriptional ActivationProgrammed cell deathTetrahydronaphthalenesmedicine.drug_classReceptors Retinoic AcidRetinoic acidAntineoplastic AgentsApoptosisBenzoateschemistry.chemical_compoundInhibitory Concentration 50RetinoidsDrug DiscoverymedicineTumor Cells CulturedHumansRetinoidIsoxazoleCytotoxicityReceptorCell DifferentiationIsoxazolesIn vitroDrug Resistance MultipleBiochemistrychemistryApoptosisDrug Resistance NeoplasmMolecular MedicineDrug Screening Assays AntitumorCell DivisionJournal of medicinal chemistry
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Plasmodium falciparumMalaria: Reduction of Endothelial Cell Apoptosis In Vitro

2005

ABSTRACTOrgan failure inPlasmodium falciparummalaria is associated with neutrophil activation and endothelial damage. This study investigates whether neutrophil-induced endothelial damage involves apoptosis and whether it can be prevented by neutralization of neutrophil secretory products. Endothelial cells from human umbilical veins were coincubated with neutrophils from healthy donors and with sera from eight patients withP. falciparummalaria, three patients withP. vivaxmalaria, and three healthy controls. Endothelial apoptosis was demonstrated by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) and annexin V staining. The rate of apoptosis of cells was …

Umbilical VeinsProgrammed cell deathEndotheliumNeutrophilsPlasmodium falciparumImmunologyApoptosisBiologyMicrobiologyAntioxidantsAnnexinparasitic diseasesmedicineAnimalsHumansProtease InhibitorsMalaria FalciparumCells CulturedTUNEL assayImmune SeraEndothelial CellsPlasmodium falciparummedicine.diseaseAscorbic acidbiology.organism_classificationEndothelial stem cellInfectious Diseasesmedicine.anatomical_structureImmunologyParasitologyEndothelium VascularFungal and Parasitic InfectionsMalariaInfection and Immunity
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Depletion ofL-arginine induces autophagy as a cytoprotective response to endoplasmic reticulum stress in human T lymphocytes

2012

PMCID: PMC3494587

X-Box Binding Protein 1Proteasome Endopeptidase ComplexProgrammed cell deathXBP1CD3 ComplexMAP Kinase Signaling SystemRNA SplicingT-LymphocytesT cellDown-RegulationApoptosisRegulatory Factor X Transcription FactorsUbiquitin-Activating EnzymesProtein Serine-Threonine KinasesBiologyArginineLymphocyte ActivationAutophagy-Related Protein 7Jurkat cellsJurkat CellsEndoribonucleasesAutophagymedicineHumansMolecular BiologyCell ProliferationTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCell BiologyBECN1Endoplasmic Reticulum StressG1 Phase Cell Cycle CheckpointsBasic Research Paper3. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureCytoprotectionApoptosisUnfolded protein responseBeclin-1MitogensApoptosis Regulatory ProteinsLysosomesProto-Oncogene Proteins c-aktTranscription FactorsAutophagy
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Targeting NUPR1 with the Small Compound ZZW-115 Is an Efficient Strategy to Treat Hepatocellular Carcinoma

2020

International audience; HCC is a highly lethal malignancy with Sorafenib as the only molecularly targeted drug. The multifunctional stress-associated protein, NUPR1, plays an essential role in controlling cell growth, migration, invasion and Sorafenib resistance in HCC. We report here that NUPR1 expression is absent in healthy liver and it is progressively upregulated in HCC premalignant lesions such as hepatitis and cirrhosis with a maximum expression in HCC samples, highlighting that NUPR1 is a potential drug target for HCC. We therefore assessed in this work, ZZW-115, a strong inhibitor of NUPR1, as a promising candidate for the treatment of HCC. We validated its extraordinary antitumor …

ZZW-1150301 basic medicineSorafenibCancer ResearchProgrammed cell deathNecrosisApoptosis InhibitorNecroptosis[SDV]Life Sciences [q-bio]Apoptosis[SDV.CAN]Life Sciences [q-bio]/Cancer03 medical and health sciences0302 clinical medicineHepatocellular Carcinoma (HCC)medicineneoplasmsComputingMilieux_MISCELLANEOUSApoptosis HCC Necroptosis NUPR1 ZZW-115Cell growthbusiness.industrymedicine.diseasedigestive system diseases3. Good health030104 developmental biologyOncologyApoptosis030220 oncology & carcinogenesisHepatocellular carcinomaNecroptosisCancer researchmedicine.symptombusinessNUPR1medicine.drug
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Des canaux Ioniques de la membrane plasmique lors de la mort cellulaire programmée induite par l’ozone chez A. thaliana

2011

Tropospheric ozone is a major secondary pollutant. In addition to its role in greenhouse effect gas, ozone is one of the most toxic air pollutants, and its pollution affects both human health and crop productivity. The work presented in this thesis concerns the role of ion channels in the plasma membrane in response to acute exposure to ozone and their interactions with signaling events leading to O3-induced PCD in A. Thaliana cultured cells. We have shown that cell death was genetically controlled and characterized by cell shrinkage similar to the mechanism of "Apoptosis Volume Decrease" (AVD) described in animal. This process is initially promoted by an early activation of a plasma membra…

[SDV.SA]Life Sciences [q-bio]/Agricultural sciences[SDV.SA] Life Sciences [q-bio]/Agricultural sciencesCanaux ioniquesOzoneArabidopsis thalianaSignalisation cellulaireIon channelsCalciumROSMort cellulaire programméeProgrammed cell deathCell signalling
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