Search results for "Fas Ligand Protein"

showing 10 items of 28 documents

Placenta-derived CD95 ligand causes liver damage in hemolysis, elevated liver enzymes, and low platelet count syndrome.

2004

Background & Aims: The HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome is a life-threatening complication during pregnancy. The associated liver disease may be severe, and maternal hepatic complications may progress to the point that transplantation becomes necessary. CD95 (APO-1, Fas)-mediated apoptosis of liver cells is one of the major pathogenic mechanisms during liver disease. The interaction of CD95 with its ligand, CD95L(FasL), induces apoptosis and thus the source of the death-inducing ligand is critical for understanding the pathomechanism of liver damage involving the CD95-system. Methods: Sera from HELLP patients were analyzed and used in cell culture experiment…

medicine.medical_specialtyHELLP SyndromeFas Ligand ProteinHELLP syndromePlacentaApoptosisBiologyHepatic ComplicationFas ligandAcute fatty liver of pregnancyLiver diseaseJurkat CellsMicePregnancyInternal medicinemedicineAnimalsHumansCells CulturedTransaminasesMembrane GlycoproteinsHepatologymedicine.diagnostic_testLiver cellGastroenterologymedicine.diseaseHemolysisMolecular WeightEndocrinologyLiverCancer researchHepatocytesFemaleLiver function testsGastroenterology
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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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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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Lymphocyte apoptosis in children with central nervous system tuberculosis: a case control study

2011

Abstract Background Studies of the apoptosis mechanisms involved in the pathogenesis of tuberculosis have suggested that Mycobacterium tuberculosis can actively interfere with the apoptosis of infected cells. In vivo studies have been performed in adult populations but have not focused on this process in children. In the present study, we analyzed spontaneous T lymphocyte (PBT) apoptosis in the peripheral blood of children with central nervous system tuberculosis (CNS TB), before and after chemotherapy, and compared the results with healthy controls. Methods A case-control study was conducted from January 2002 to June 2009. It included 18 children with CNS TB and 17 healthy controls. Sponta…

Central Nervous SystemMaleFas Ligand ProteinTuberculosisSettore MED/17 - Malattie InfettiveTuberculosiT-Lymphocytesmedicine.medical_treatmentCentral nervous systemApoptosisLymphocyte ActivationMycobacterium tuberculosisPathogenesismeningoencephalitichildrenCentral Nervous System Bacterial InfectionsmedicineHumansfas ReceptorPediatrics Perinatology and Child HealthChildSettore MED/04 - Patologia GeneraleChemotherapybiologybusiness.industrylcsh:RJ1-570Case-control studylcsh:PediatricsMycobacterium tuberculosisT lymphocyteTuberculosis Central Nervous Systembiology.organism_classificationmedicine.diseaseapoptosimedicine.anatomical_structureApoptosisCase-Control StudiesChild PreschoolPediatrics Perinatology and Child HealthImmunologyFemalebusinessResearch ArticleBMC Pediatrics
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Declining Physical Performance Associates with Serum FasL, miR-21, and miR-146a in Aging Sprinters.

2016

Aging is associated with systemic inflammation and cellular apoptosis accelerating physiological dysfunctions. Whether physically active way of life affects these associations is unclear. This study measured the levels of serum inflammatory and apoptotic molecules, their change over 10 years, and their associations with physical performance in sprint-trained male athletes. HsCRP, cell counts, HGB, FasL, miR-21, and miR-146a were measured cross-sectionally (n=67, 18–90 yrs) and serum FasL, miR-21, and miR-146a and their aging-related associations with physical performance were assessed over a 10-year follow-up (n=49, 50–90 yrs). The cross-sectional study showed positive age correlations for …

0301 basic medicineMaleAgingCelllcsh:MedicineSystemic inflammationBench pressFas ligandRunning0302 clinical medicineYoung adultpikajuoksijatAged 80 and overta3141General Medicineinflammatory responseMiddle Agedmedicine.anatomical_structuremedicine.symptomInflammation MediatorsResearch ArticleAdultmedicine.medical_specialtyFas Ligand ProteinArticle SubjectAdolescentGeneral Biochemistry Genetics and Molecular Biologysprinters03 medical and health sciencesYoung AdultInternal medicinemedicineHumansAgedGeneral Immunology and Microbiologybusiness.industryaginglcsh:R030229 sport sciencesphysical performanceCirculating MicroRNAMicroRNAs030104 developmental biologyEndocrinologyCross-Sectional StudiesPhysical performanceApoptosisPhysical FitnessImmunologybusinessBiomarkersFollow-Up StudiesBioMed research international
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Defective apoptosis and tumorigenesis: role of p53 mutation and Fas/FasL system dysregulation

2010

The transcription factor p53 and the cytokine receptor FasL are two of the most famous regulators of cell life, and their alterations can cause a large number of pathologies, including cancer. In this review, we focused on how they can determine defective apoptosis, one of the causes of tumorigenesis and tumor progression. The importance of this knowledge lies in the new perspectives that gene therapy can offer to cure cancer.

Fas Ligand ProteinHistologyFree RadicalsCellBiophysicsApoptosisBiologymedicine.disease_causeFas ligandNeoplasmsmedicineAnimalsHumansfas ReceptorTranscription factorlcsh:QH301-705.5Membrane GlycoproteinsfungiCancerfood and beveragesGenetic TherapyCell BiologyGenes p53medicine.diseaseGenes bcl-2medicine.anatomical_structurelcsh:Biology (General)ApoptosisTumor progressionImmunologyCarcinogenesisCytokine receptorEuropean Journal of Histochemistry
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Enhancing production and cytotoxic activity of polymeric soluble FasL-based chimeric proteins by concomitant expression of soluble FasL.

2012

International audience; Membrane FasL is the natural trigger of Fas-mediated apoptosis. A soluble homotrimeric counterpart (sFasL) also exists which is very weakly active, and needs oligomerization beyond its trimeric state to induce apoptosis. We recently generated a soluble FasL chimera by fusing the immunoglobulin-like domain of the leukemia inhibitory factor receptor gp190 to the extracellular region of human FasL, which enabled spontaneous dodecameric homotypic polymerization of FasL. This polymeric soluble human FasL (pFasL) displayed anti-tumoral activity in vitro and in vivo without systemic cytotoxicity in mouse. In the present work, we focused on the improvement of pFasL, with two…

Fas Ligand Proteinlcsh:MedicineLeukemia inhibitory factor receptorEnzyme-Linked Immunosorbent AssayBiologyPolymerase Chain ReactionFas ligandChimera (genetics)Biopolymers[ SDV.MP ] Life Sciences [q-bio]/Microbiology and ParasitologyCytotoxic T cellHumanslcsh:Science[SDV.MP] Life Sciences [q-bio]/Microbiology and ParasitologyDNA PrimersMultidisciplinaryBase SequenceT-cell receptorlcsh:RTransfectionFusion proteinMolecular biologyIn vitroCell biologySolubilitylcsh:QResearch Article
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Lack of association between gene polymorphisms of Angiotensin converting enzyme, Nod-like receptor 1, Toll-like receptor 4, FAS/FASL and the presence…

2011

Abstract Background Several polymorphisms of genes involved in the immunological recognition of Helicobacter pylori and regulating apoptosis and proliferation have been linked to gastric carcinogenesis, however reported data are partially conflicting. The aim of our study was to evaluate potential associations between the presence of gastric cancer (GC) and high risk atrophic gastritis (HRAG) and polymorphisms of genes encoding Angiotensin converting enzyme (ACE), Nod-like receptor 1 (NOD1), Toll-like receptor 4 (TLR4) and FAS/FASL. Methods Gene polymorphisms were analyzed in 574 subjects (GC: n = 114; HRAG: n = 222, controls: n = 238) of Caucasian origin. ACE I/D (rs4646994), NOD1 796G&gt;…

AdultGastritis AtrophicMaleFas Ligand ProteinGenotypeAtrophic gastritisPeptidyl-Dipeptidase AWhite PeopleFas ligandHelicobacter InfectionsRisk FactorsStomach NeoplasmsNod1 Signaling Adaptor ProteinNOD1GenotypemedicineGeneticsHumansGenetics(clinical)fas ReceptorAllelesGenetics (clinical)AgedAged 80 and overPolymorphism GeneticHelicobacter pyloribiologyCancerAngiotensin-converting enzymeMiddle AgedHelicobacter pylorimedicine.diseasebiology.organism_classificationToll-Like Receptor 4ApoptosisImmunologybiology.proteinFemalePrecancerous ConditionsResearch ArticleBMC Medical Genetics
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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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