Search results for "FAS ligand"

showing 10 items of 51 documents

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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Hyperthermia Enhances CD95-Ligand Gene Expression in T Lymphocytes

2004

Abstract Hyperthermia represents an interesting therapeutic strategy for the treatment of tumors. Moreover, it is able to regulate several aspects of the immune response. Fas (APO-1/CD95) and its ligand (FasL) are cell surface proteins whose interaction activates apoptosis of Fas-expressing targets. In T cells, the Fas-Fas-L system regulates activation-induced cell death, is implicated in diseases in which lymphocyte homeostasis is compromised, and plays an important role during cytotoxic and regulatory actions mediated by these cells. In this study we describe the effect of hyperthermia on activation of the fas-L gene in T lymphocytes. We show that hyperthermic treatment enhances Fas-L-med…

HyperthermiaFas Ligand ProteinFeverT-LymphocytesT cellBlotting WesternImmunologyBiologyLymphocyte ActivationTransfectionFas ligandJurkat CellsTransactivationImmune systemHeat Shock Transcription FactorsLymphocyte homeostasismedicineAnimalsHumansImmunology and AllergyCytotoxic T cellRNA MessengerPromoter Regions GeneticTranscription factorProtein Kinase CMembrane GlycoproteinsNF-kappa BBlotting NorthernCytotoxicity Tests Immunologicmedicine.diseaseMolecular biologyCell biologyDNA-Binding ProteinsTranscription Factor AP-1medicine.anatomical_structureGene Expression RegulationMutationTranscription FactorsThe Journal of Immunology
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Response to 'Thyrocytes — not innocent bystanders in autoimmune disease'

2001

Giordano et al. propose that thyrocytes play a crucial role in the regulation of the autoimmune response during GD. According to them, Fas is weakly expressed in GD thyrocytes, whereas FasL is responsible for a specific deletion of infiltrating TH1 cells and maintains a TH2 phenotype in the lymphocytic infiltrate.

Lymphocytic InfiltrateAutoimmune diseaseImmunologyImmunologymedicineImmunology and AllergyBiologymedicine.diseasePhenotypeFas ligandNature Immunology
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S-nitrosylation of the death receptor fas promotes fas ligand-mediated apoptosis in cancer cells.

2011

International audience; BACKGROUND & AIMS: Fas belongs to the family of tumor necrosis factor receptors which induce apoptosis. Many cancer cells express Fas but do not undergo Fas-mediated apoptosis. Nitric oxide reverses this resistance by increasing levels of Fas at the plasma membrane. We studied the mechanisms by which NO affects Fas function. METHODS: Colon and mammary cancer cell lines were incubated with the NO donor glyceryl trinitrate or lipid A; S-nitrosylation of Fas was monitored using the biotin switch assay. Fas constructs that contained mutations at cysteine residues that prevent S-nitrosylation were used to investigate the involvement of S-nitrosylation in Fas-mediated cell…

MESH: NitroglycerinMESH: Signal TransductionTime FactorsMESH: Membrane MicrodomainsApoptosisMESH : Fas Ligand ProteinCytoplasmic partMESH: Lipid AFas ligandMiceNitroglycerin0302 clinical medicineMESH : Protein TransportMESH : FemaleMESH: AnimalsFADDLipid raft0303 health sciencesTumorbiologyColon CancerMESH : Lipid AMESH : BiotinylationGastroenterologyFas receptorMESH: Antigens CD95Protein TransportLipid AMESH : Colonic NeoplasmsMESH : Nitric OxideMESH : Nitric Oxide Donors030220 oncology & carcinogenesisColonic NeoplasmsDeath-inducing signaling complexFemale[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH : MutationMESH : TransfectionSignal TransductionMESH : Time FactorsMESH: Protein TransportFas Ligand ProteinMESH : Mammary Neoplasms ExperimentalMESH: MutationMESH: Cell Line TumorMESH: Mammary Neoplasms ExperimentalNitric OxideTransfectionCaspase 803 medical and health sciencesMembrane MicrodomainsCell Line TumorMESH : MiceAnimalsHumansBiotinylationNitric Oxide DonorsMESH: BiotinylationCysteinefas ReceptorMESH: MiceMESH : Protein Processing Post-Translational030304 developmental biologyMESH : Signal TransductionMESH: Colonic NeoplasmsMESH : CysteineMESH: HumansHepatologyMESH : Cell Line TumorMESH: ApoptosisMESH: TransfectionMESH : HumansMESH: Time FactorsMammary Neoplasms Experimental[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: CysteineMESH: Nitric Oxide DonorsMolecular biologySignalingMESH: Fas Ligand ProteinMESH : NitroglycerinApoptosisLocalizationMESH: Nitric OxideMESH: Protein Processing Post-TranslationalMutationbiology.proteinMESH : Membrane MicrodomainsMESH : AnimalsMESH : Antigens CD95Protein Processing Post-TranslationalMESH: FemaleMESH : Apoptosis
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Apoptosis in malignant glioma cells triggered by the temozolomide-induced DNA lesion O6-methylguanine

2006

Methylating drugs such as temozolomide (TMZ) are widely used in the treatment of brain tumours (malignant gliomas). The mechanism of TMZ-induced glioma cell death is unknown. Here, we show that malignant glioma cells undergo apoptosis following treatment with the methylating agents N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and TMZ. Cell death determined by colony formation and apoptosis following methylation is greatly stimulated by p53. Transfection experiments with O(6)-methylguanine-DNA methyltransferase (MGMT) and depletion of MGMT by O(6)-benzylguanine showed that, in gliomas, the apoptotic signal originates from O(6)-methylguanine (O(6)MeG) and that repair of O(6)MeG by MGMT prevent…

MethylnitronitrosoguanidineCancer ResearchProgrammed cell deathFas Ligand ProteinGuanineDNA repairFas-Associated Death Domain ProteinBlotting WesternApoptosisBiologymedicine.disease_causeO(6)-Methylguanine-DNA MethyltransferaseGliomaTemozolomideTumor Cells CulturedGeneticsmedicineHumansDNA Breaks Double-StrandedRNA Small InterferingAntineoplastic Agents AlkylatingneoplasmsMolecular BiologyTumor Stem Cell AssayCell ProliferationTemozolomideBrain NeoplasmsCell CycleGliomaCell cycleFlow CytometryFas receptormedicine.diseaseDacarbazineProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesCancer researchTumor Suppressor Protein p53CarcinogenesisDNA Damagemedicine.drugOncogene
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Pharmacogenomics of cantharidin in tumor cells.

2014

Cantharis vesicatoria (blister beetle) is used in Chinese medicine and has been categorized as highly toxic in the Chinese pharmacopeia. In Europe, Cantharis patches have been used since ages to treat various skin-related diseases. We investigated the cytotoxicity of the Cantharis ingredient, cantharidin, in 41 tumor cell lines (Oncotest panel) and compared the results with those of 60 cell lines of the National Cancer Institute, USA. We found profound activity at low micromolar concentrations (log ₁₀IC₅₀ values between -6.980 and 5.009 M). Cantharidin bound to protein phosphatase 2A (PP2A) with higher affinity (-8.12 kcal/mol) than to PP1 (-6.25 kcal/mol) in molecular docking analyses. Usi…

Models MolecularProtein ConformationBlister beetleBiologyCantharisBiochemistryFas ligandGene Expression Regulation Enzymologicchemistry.chemical_compoundCell Line TumorGene expressionAnimalsHumansRNA MessengerCytotoxicityOligonucleotide Array Sequence AnalysisPharmacologyCantharidinBinding SitesMolecular Structurebiology.organism_classificationMolecular biologyReceptors Neuropeptide YchemistryCell cultureApoptosisPharmacogeneticsImmunologyCantharidinBiochemical pharmacology
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Deglycosylated bleomycin induces apoptosis in lymphoma cell via c-jun NH2-terminal kinase but not reactive oxygen species

2007

Bleomycin (BLM) has demonstrated potent activity in treating malignant lymphomas but its therapeutic efficacy is hampered by induction of lung fibrosis. This side effect is related to the ability of the drug to generate reactive oxygen species in lung cells. In the present study, we evaluated the consequences of deglycosylation of BLM in term of cytotoxic activity and generation of reactive oxygen species. When tested on U937 human lymphoma cells, both compounds generated a typical apoptotic phenotype. Cell death induction was associated with Bax oligomerization, dissipation of the mitochondrial membrane potential, release of cytochrome c, caspase activation, chromatin condensation and inte…

Programmed cell deathFas Ligand ProteinLymphomaCellApoptosisDNA FragmentationBiologymedicine.disease_causeBiochemistryTNF-Related Apoptosis-Inducing LigandBleomycinmedicineHumansDeath domainPharmacologychemistry.chemical_classificationReactive oxygen speciesAntibiotics AntineoplasticU937 cellCytochrome cJNK Mitogen-Activated Protein KinasesU937 CellsMolecular biologymedicine.anatomical_structurechemistryBiochemistryApoptosisCaspasesbiology.proteinReactive Oxygen SpeciesOxidative stressBiochemical Pharmacology
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Role Of S-Nitrosylation In The Extrinsic Apoptotic Signalling Pathway In Cancer.

2015

One of the key features of tumour cells is the acquisition of resistance to apoptosis. Thus, determining therapeutic strategies that circumvent apoptotic resistance and result in tumor regression is a challenge. One strategy to induce apoptosis is to activate death receptor signalling pathways. Members of the Tumor Necrosis Factor TNF-family death receptors ligand (TRAIL, FasL and TNF-α) can originate from immune and non-immune cells. Death receptors, engaged by cognate ligands, can initiate multiple signaling pathways, which can generate diverse outcomes, including non-apoptosis-related signal. Knowledge on the molecular mechanisms (that determine death or survival of tumour cells) followi…

Programmed cell deathlcsh:R5-920Organic ChemistryClinical BiochemistryApoptosisS-NitrosylationBiologyCell fate determinationNitric OxideBiochemistryFas ligandCell biologyNeoplasm Proteinslcsh:Biology (General)ApoptosisCell Line TumorNeoplasmsAnimalsHumansTumor necrosis factor alphaSignal transductionReceptorlcsh:Medicine (General)lcsh:QH301-705.5Signal TransductionRedox biology
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Apoptosis in liver disease

2001

A variety of biological functions are regulated through extracellular signals. Amongst the best studied examples is growth control, which is achieved by the regulatory function of growth factors. In recent years it has become apparent that cell death (apoptosis) is controlled in a similar fashion. Apoptosis, firstly a morphologically defined process, is a highly controlled type of cell death that plays a critical role in embryonic development, deletion of autoreactive T-cells and adult tissue homoeostasis. There is increasing evidence that derangement of the apoptotic program is the underlying cause of a series of diseases including liver diseases. The deadly program can be initiated by lig…

ProteasesProgrammed cell deathApoptosisLigandsReceptors Tumor Necrosis FactorFas ligandTransforming Growth Factor beta1Antigens CDTransforming Growth Factor betaExtracellularAnimalsHumansfas ReceptorCaspaseHepatologybiologyLiver DiseasesGastroenterologyFas receptorCell biologyBiochemistryReceptors Tumor Necrosis Factor Type IApoptosisCaspasesbiology.proteinIntracellularEuropean Journal of Gastroenterology &amp; Hepatology
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Circulating miR-21, miR-146a and Fas ligand respond to postmenopausal estrogen-based hormone replacement therapy--a study with monozygotic twin pairs.

2014

Biological aging is associated with physiological deteriorations and its’ remodeling, which are partly due to changes in the hormonal profile. MicroRNAs are known to post-transcriptionally regulate various cellular processes associated with cell senescence; differentiation, replication and apoptosis. Measured from the serum, microRNAs have the potential to serve as noninvasive markers for diagnostics/prognostics and therapeutic targets. We analysed the association of estrogen-based hormone replacement therapy (HRT) with selected microRNAs and inflammation markers from the serum, leukocytes and muscle tissue biopsy samples obtained from 54-62 year-old postmenopausal monozygotic twins (n=11 p…

SenescenceAdultmedicine.medical_specialtyAgingFas Ligand Proteinmedicine.drug_classmedicine.medical_treatmentMonozygotic twinInflammationApoptosisBiologyta3111Fas ligand“Inflamm-aging”Internal medicinemicroRNAmedicineestrogenHumansmicrornasMuscle SkeletalHormone therapyCellular SenescenceInflammationmicroRNAEstrogen Replacement TherapyapoptosisHormone replacement therapy (menopause)ta3141Cell DifferentiationEstrogenstwinsTwins MonozygoticMiddle AgedPostmenopauseAgeinghormone replacement therapyMicroRNAsEndocrinologyEstrogenFemalemedicine.symptomBiomarkersDevelopmental BiologyHormoneMechanisms of ageing and development
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