Search results for "CD95"

showing 9 items of 9 documents

Studio dell'apoptosi cellulare nella pre-eclampsia mediante valutazione del CD95 linfocitario in pazienti trattate con antitrombina III

2009

L'etimologia della pre-eclampsia rimane ancora oggi sconosciuta ma sappiamo abbastanza sulla sua fisiopatologia, da consentire l'adozione di presidi terapeutici atti ad espletare un controllo sintomatologico della sindrome ma non a curarla. Nel presente lavoro ci siamo posti l'obiettivo di valutare in corso di trattamento con ATIII l'andamento dei valori di CD95 dei linfociti del circolo periferico, in qualità di indicatore dei processi di apoptosi cellulare in una condizione di "Graft versus host disease", quale potrebbe considerarsi la gravidanza complicata da pre-eclampsia.

apoptosi cellulare valutazione del CD95 antitrombinaSettore MED/40 - Ginecologia E Ostetricia
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Missense mutations in the fas gene resulting in autoimmune lymphoproliferative syndrome: A molecular and immunological analysis

1997

AbstractProgrammed cell death (or apoptosis) is a physiological process essential to the normal development and homeostatic maintenance of the immune system. The Fas/Apo-1 receptor plays a crucial role in the regulation of apoptosis, as demonstrated by lymphoproliferation in MRL-lpr/lpr mice and by the recently described autoimmune lymphoproliferative syndrome (ALPS) in humans, both of which are due to mutations in the Fas gene. We describe a novel family with ALPS in which three affected siblings carry two distinct missense mutations on both the Fas gene alleles and show lack of Fas-induced apoptosis. The children share common clinical features including splenomegaly and lymphadenopathy, b…

Antigens Differentiation T-LymphocyteMaleAdolescentT-LymphocytesCD3ImmunologyLymphoproliferative disordersBiologyLymphocyte ActivationAutoimmune DiseaseBiochemistryFas ligandImmunophenotypingImmune systemPedigree; Antigens Differentiation T-Lymphocyte; Solubility; Apoptosis; Autoimmune Diseases; Humans; Antigens CD95; Child; Lymphocytes; Child Preschool; Lymphocyte Activation; Syndrome; Lymphoproliferative Disorders; Adolescent; Mutation; Immunophenotyping; Male; Biological Markers; T-LymphocytesmedicineChildAutoimmune diseaseApoptosiSyndromeCell BiologyHematologymedicine.diseaseFas receptorPedigreeAntigens CD95SolubilityApoptosisChild PreschoolLymphoproliferative DisorderAutoimmune lymphoproliferative syndromeMutationBiological MarkerImmunologybiology.proteinLymphocyteHuman
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The novel NF-κB inhibitor DHMEQ synergizes with celecoxib to exert antitumor effects on human liver cancer cells by a ROS-dependent mechanism

2012

In a previous work of ours dehydroxymethyl-epoxyquinomicin (DHMEQ), an inhibitor of NF-κB, was shown to induce apoptosis through Reactive Oxygen Species (ROS) production in hepatoma cells. The present study demonstrated that DHMEQ cooperates with Celecoxib (CLX) to decrease NF-κB DNA binding and to inhibit cell growth and proliferation more effectively than treatment with these single agents alone in the hepatoma cell lines HA22T/VGH and Huh-6. ROS production induced by the DHMEQ-CLX combination in turn generated the expression of genes involved in endoplasmic reticulum (ER) stress and silencing TRB3 mRNA significantly decreased DHMEQ-CLX-induced cell growth inhibition. Moreover, the DHMEQ-…

Cancer ResearchCarcinoma HepatocellularAntineoplastic AgentsApoptosisCell Cycle ProteinsProtein Serine-Threonine KinasesBiologyDHMEQ Celecoxib NF-jB CD95/CD95L Liver cancer cellsCell Line TumorSurvivinHumansGene silencingfas ReceptorProtein kinase BCell ProliferationSulfonamidesGene knockdownCyclooxygenase 2 InhibitorsCyclohexanonesCell growthEndoplasmic reticulumLiver NeoplasmsNF-kappa BDrug SynergismEndoplasmic Reticulum StressMolecular biologyAcetylcysteineRepressor ProteinsOncologyCelecoxibCell cultureApoptosisBenzamidesCancer researchPyrazolesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesCancer Letters
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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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CD95 DISC formation and internalizzation occur in lipid rafts of typeI and typeII cells

2004

We investigated the membrane localization of CD95 in type I and type II cells, which differ in their ability to recruit and activate caspase-8. We found that CD95 was preferentially located in lipid rafts of type I cells, while it was present both in raft and non-raft plasma membrane sub-domains of type II cells. After stimulation, CD95 located in phospholipid-rich plasma membrane was recruited to lipid rafts in both types of cells. Similarly, CD95 cross-linking resulted in caspase-independent translocation of FADD/MORT1 and caspase-8 to the lipid rafts, which was prevented by a death domain-defective receptor. CD95 internalization was then rapid in type I and delayed in type II cells and s…

CD95Caspase-8Lipid rafts
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CNS Macrophages Control Neurovascular Development via CD95L.

2017

The development of neurons and vessels shares striking anatomical and molecular features, and it is presumably orchestrated by an overlapping repertoire of extracellular signals. CNS macrophages have been implicated in various developmental functions, including the morphogenesis of neurons and vessels. However, whether CNS macrophages can coordinately influence neurovascular development and the identity of the signals involved therein is unclear. Here, we demonstrate that activity of the cell surface receptor CD95 regulates neuronal and vascular morphogenesis in the post-natal brain and retina. Furthermore, we identify CNS macrophages as the main source of CD95L, and macrophage-specific del…

0301 basic medicineFas Ligand ProteinAngiogenesisMorphogenesisvesselmicrogliaBiologyGeneral Biochemistry Genetics and Molecular BiologyRetina03 medical and health sciencesangiogenesisMiceCell surface receptorExtracellularmedicineHuman Umbilical Vein Endothelial CellsNeuritesAnimalsHumansfas Receptorlcsh:QH301-705.5Cell ProliferationRetinaMicrogliaKinaseMacrophagesneurovascular developmentBrainNeurovascular bundle030104 developmental biologymedicine.anatomical_structurecortexsrc-Family Kinasesnervous systemlcsh:Biology (General)ImmunologySynapsesCD95CD95LNeuroscienceCNS macrophagesProtein BindingSignal TransductionCell reports
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Downregulation of thioredoxin-1-dependent CD95 S-nitrosation by Sorafenib reduces liver cancer

2020

Hepatocellular carcinoma (HCC) represents 80% of the primary hepatic neoplasms. It is the sixth most frequent neoplasm, the fourth cause of cancer-related death, and 7% of registered malignancies. Sorafenib is the first line molecular targeted therapy for patients in advanced stage of HCC. The present study shows that Sorafenib exerts free radical scavenging properties associated with the downregulation of nuclear factor E2-related factor 2 (Nrf2)-regulated thioredoxin 1 (Trx1) expression in liver cancer cells. The experimental downregulation and/or overexpression strategies showed that Trx1 induced activation of nitric oxide synthase (NOS) type 3 (NOS3) and S-nitrosation (SNO) of CD95 rece…

0301 basic medicine:Anatomy::Cells::Cells Cultured::Cell Line::Cell Line Tumor [Medical Subject Headings]Factor 2 relacionado con NF-E2Regulación hacia abajomedicine.medical_treatment[SDV]Life Sciences [q-bio]Clinical Biochemistry:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Thioredoxins [Medical Subject Headings]ApoptosisBiochemistry:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Nitrosation [Medical Subject Headings]Targeted therapyNeoplasias hepáticas:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]Mice0302 clinical medicineThioredoxins:Organisms::Eukaryota::Animals [Medical Subject Headings]lcsh:QH301-705.5Cell proliferationlcsh:R5-920GSNORChemistry:Diseases::Neoplasms::Neoplasms by Site::Digestive System Neoplasms::Liver Neoplasms [Medical Subject Headings]Liver NeoplasmsSorafenibFas receptor3. Good healthHepatocellular carcinomaCD95Liver cancerlcsh:Medicine (General)NOS3Liver cancerCarcinoma hepatocelularResearch Papermedicine.drugSorafenibHepatocarcinomaProliferación celularCarcinoma HepatocellularNitrosationDown-RegulationMice Nude[SDV.CAN]Life Sciences [q-bio]/CancerAntineoplastic AgentsNrf203 medical and health sciencesDownregulation and upregulationCell Line TumormedicineAnimalsHumansS-NitrosoglutatiónTiorredoxinas:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Mice [Medical Subject Headings]:Diseases::Neoplasms::Neoplasms by Site::Digestive System Neoplasms::Liver Neoplasms::Carcinoma Hepatocellular [Medical Subject Headings]:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Down-Regulation [Medical Subject Headings]Cell growthPhenylurea CompoundsOrganic Chemistry:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Antineoplastic Agents [Medical Subject Headings][SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Mice::Mice Mutant Strains::Mice Nude [Medical Subject Headings]medicine.diseasedigestive system diseases030104 developmental biologylcsh:Biology (General)ApoptosisDownregulation:Chemicals and Drugs::Organic Chemicals::Hydrocarbons::Hydrocarbons Cyclic::Hydrocarbons Aromatic::Benzene Derivatives::Phenylurea Compounds [Medical Subject Headings][SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyCancer researchÓxido nítrico sintasa de tipo III030217 neurology & neurosurgery
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Defective stromal remodeling and neutrophil extracellular traps in lymphoid tissues favor the transition from autoimmunity to lymphoma

2013

Abstract Altered expression of matricellular proteins can become pathogenic in the presence of persistent perturbations in tissue homeostasis. Here, we show that autoimmunity associated with Fas mutation was exacerbated and transitioned to lymphomagenesis in the absence of SPARC (secreted protein acidic rich in cysteine). The absence of SPARC resulted in defective collagen assembly, with uneven compartmentalization of lymphoid and myeloid populations within secondary lymphoid organs (SLO), and faulty delivery of inhibitory signals from the extracellular matrix. These conditions promoted aberrant interactions between neutrophil extracellular traps and CD5+ B cells, which underwent malignant …

MyeloidLymphoid Tissue: immunologyLymphomaNeutrophilsChronic lymphocytic leukemiaAutoimmunityOsteonectin: geneticsCHRONIC LYMPHOCYTIC-LEUKEMIA; SYSTEMIC-LUPUS-ERYTHEMATOSUS; INHIBITORY RECEPTOR LAIR-1; KAPPA-B ACTIVATION; MARGINAL ZONE; INFLAMMATORY DISORDERS; MATRICELLULAR PROTEIN; SPARCMalignant transformationExtracellular matrixKAPPA-B ACTIVATIONLymphoma: immunologyMicehemic and lymphatic diseasesOsteonectinSYSTEMIC-LUPUS-ERYTHEMATOSUSNF-kappa B: immunologyCells CulturedTissue homeostasisB-LymphocytesCulturedNF-kappa BLymphoid Tissue: cytologyCell biologyCD5: immunologyExtracellular MatrixMutant Strainsmedicine.anatomical_structureINHIBITORY RECEPTOR LAIR-1OncologyCD95Stromal cellLymphoid TissueCellsBiologyCD95: geneticsCD5 AntigensINFLAMMATORY DISORDERSExtracellular Matrix: immunologymedicineAnimalsHumansfas ReceptorAntigensB-Lymphocytes: immunologyMATRICELLULAR PROTEINCHRONIC LYMPHOCYTIC-LEUKEMIASPARCLymphoma: geneticsNeutrophil extracellular trapsmedicine.diseaseAnimals; Antigens; Autoimmunity; B-Lymphocytes; B-Lymphocytes: immunology; CD5; CD5: immunology; CD95; CD95: genetics; Cells; Cultured; Extracellular Matrix; Extracellular Matrix: immunology; Humans; Lymphoid Tissue; Lymphoid Tissue: cytology; Lymphoid Tissue: immunology; Lymphoma; Lymphoma: genetics; Lymphoma: immunology; Mice; Mutant Strains; NF-kappa B; NF-kappa B: immunology; Neutrophils; Neutrophils: immunology; Osteonectin; Osteonectin: genetics; Osteonectin: immunologyMice Mutant StrainsCD5Neutrophils: immunologyOsteonectin: immunologyMARGINAL ZONELymphoma SPARC autoimmunityCD5
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CD95 death-inducing signaling complex formation and internalization occur in lipid rafts of type I and type II cells

2004

We investigated the membrane localization of CD95 in type I and type II cells, which differ in their ability to recruit and activate caspase-8. We found that CD95 was preferentially located in lipid rafts of type I cells, while it was present both in raft and non-raft plasma membrane sub-domains of type II cells. After stimulation, CD95 located in phospholipid-rich plasma membrane was recruited to lipid rafts in both types of cells. Similarly, CD95 cross-linking resulted in caspase-independent translocation of FADD/MORT1 and caspase-8 to the lipid rafts, which was prevented by a death domain-defective receptor. CD95 internalization was then rapid in type I and delayed in type II cells and s…

Death Domain Receptor Signaling Adaptor ProteinsEndosomeT-Lymphocytesmedia_common.quotation_subjectImmunologyApoptosisReceptors Tumor Necrosis FactorCell LineMembrane MicrodomainsSettore MED/04 - PATOLOGIA GENERALECell Line TumorReceptorsHumansImmunology and Allergyfas ReceptorFADDInternalizationLipid raftLipid raftsDeath domainmedia_commonTumorbiologyVesicleFas receptorEndocytosisCell biologyProtein TransportCholesterolCD95 death-inducing signaling complexCaspasesCD95biology.proteinlipids (amino acids peptides and proteins)biological phenomena cell phenomena and immunityCaspase-8Tumor Necrosis FactorCaspase-8; CD95; Lipid rafts; Apoptosis; Caspases; Cell Line Tumor; Cholesterol; Death Domain Receptor Signaling Adaptor Proteins; Humans; Membrane Microdomains; Protein Binding; Protein Transport; Receptors Tumor Necrosis Factor; T-Lymphocytes; fas Receptor; Endocytosis; Signal Transduction; Immunology and Allergy; ImmunologyProtein BindingSignal TransductionEuropean Journal of Immunology
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