Search results for " ACTIVATION"

showing 10 items of 1535 documents

Secreted proteophosphoglycan of Leishmania mexicana amastigotes activates complement by triggering the mannan binding lectin pathway.

1997

Cutaneous lesions induced by infection of mice with the protozoan parasite, Leishmania mexicana, contain abundant amounts of a high molecular mass proteophosphoglycan (PPG), which is secreted by the amastigote stage residing in phagolysosomes of macrophages and can then be released into the tissue upon rupture of the infected cells. Amastigote PPG forms sausage-shaped but soluble particles and belongs to a novel class of serine-rich proteins that are extensively O-glycosylated by phosphooligosaccharides capped by mannooligosaccharides. The purified molecule is shown here to efficiently activate complement (C) and deplete hemolytic activity of normal serum and may prevent the opsonization of…

ImmunologyLeishmania mexicanaProtozoan ProteinsCollectinLeishmaniasis CutaneousLeishmania mexicanaMiceImmunology and AllergyAnimalsAmastigoteComplement ActivationMannan-binding lectinSerine proteaseMice KnockoutbiologyMacrophagesComplement C4Complement C3biology.organism_classificationCollectinsComplement systemAntibody opsonizationBiochemistryLectin pathwaybiology.proteinMice Inbred CBACalciumProteoglycansCarrier ProteinsEuropean journal of immunology
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Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain.

2005

Activating mutations in the FLT3 tyrosine kinase (TK) occur in approximately 35% of patients with acute myeloid leukemia (AML). Therefore, targeting mutated FLT3 is an attractive therapeutic strategy, and early clinical trials testing FLT3 TK inhibitors (TKI) showed measurable clinical responses. Most of these responses were transient; however, in a subset of patients blast recurrence was preceded by an interval of prolonged remission. The etiology of clinical resistance to FLT3-TKI in AML is unclear but is of major significance for the development of future therapeutic strategies. We searched for mechanisms of resistance in 6 patients with AML who had relapses upon PKC412 treatment. In an …

ImmunologyMutation MissenseBiologyBiochemistrychemistry.chemical_compoundIn vivoRecurrencehemic and lymphatic diseasesHumansProtein Kinase InhibitorsProtein Kinase CQuizartinibKinaseMyeloid leukemiaCell BiologyHematologyProtein-Tyrosine KinasesStaurosporineEnzyme ActivationProtein kinase domainchemistryfms-Like Tyrosine Kinase 3Drug Resistance NeoplasmLeukemia MyeloidFms-Like Tyrosine Kinase 3Acute DiseaseCancer researchTyrosine kinaseCrenolanibBlood
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A central role for Notch in effector CD8(+) T cell differentiation.

2014

Activated CD8(+) T cells choose between terminal effector cell (TEC) or memory precursor cell (MPC) fates. We found that the signaling receptor Notch controls this 'choice'. Notch promoted the differentiation of immediately protective TECs and was correspondingly required for the clearance of acute infection with influenza virus. Notch activated a major portion of the TEC-specific gene-expression program and suppressed the MPC-specific program. Expression of Notch was induced on naive CD8(+) T cells by inflammatory mediators and interleukin 2 (IL-2) via pathways dependent on the metabolic checkpoint kinase mTOR and the transcription factor T-bet. These pathways were subsequently amplified d…

ImmunologyNotch signaling pathwayMice TransgenicCell SeparationBiologyAdaptive ImmunityCD8-Positive T-LymphocytesEffector cellLymphocyte ActivationReal-Time Polymerase Chain ReactionArticlememoryMiceOrthomyxoviridae InfectionsCell surface receptorT-Lymphocyte SubsetsTransduction GeneticPrecursor cellImmunology and AllergyCytotoxic T cellAnimalsGeneticsReceptors NotchEffectorCell DifferentiationFlow CytometryAdoptive TransferTEC3. Good healthCell biologyMice Inbred C57BLeffectorCD8 T cellMPCInfluenza A virusinflammationTranscriptomeCD8Nature immunology
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Murine model of interstitial cytomegalovirus pneumonia in syngeneic bone marrow transplantation: persistence of protective pulmonary CD8-T-cell infil…

2000

ABSTRACTInterstitial pneumonia (IP) is a severe organ manifestation of cytomegalovirus (CMV) disease in the immunocompromised host, in particular in recipients of bone marrow transplantation (BMT). Diagnostic criteria for the definition of CMV-IP include clinical evidence of pneumonia together with CMV detected in bronchoalveolar lavage or lung biopsy. We have used the model of syngeneic BMT and simultaneous infection of BALB/c mice with murine CMV for studying the pathogenesis of CMV-IP by controlled longitudinal analysis. A disseminated cytopathic infection of the lungs with fatal outcome was observed only when reconstituting CD8 T cells were depleted. Neither CD8 nor CD4 T cells mediated…

ImmunologyPneumonia ViralBiologyCD8-Positive T-LymphocytesLymphocyte ActivationMicrobiologyPathogenesisMiceVirologyImmunopathologymedicineCytotoxic T cellAnimalsHumansLungBone Marrow TransplantationMice Inbred BALB CLungmedicine.diagnostic_testSyngeneic Bone Marrow TransplantationDisease Models AnimalTransplantation Isogeneicmedicine.anatomical_structureBronchoalveolar lavagePhenotypeViral replicationInsect ScienceImmunologyCytomegalovirus InfectionsPathogenesis and ImmunityFemaleLung Diseases InterstitialCD8Journal of virology
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Protection from graft-versus-host disease by HIV-1 envelope protein gp120-mediated activation of human CD4+CD25+ regulatory T cells.

2009

AbstractNaturally occurring CD4+CD25+ regulatory T cells (Tregs) represent a unique T-cell lineage that is endowed with the ability to actively suppress immune responses. Therefore, approaches to modulate Treg function in vivo could provide ways to enhance or reduce immune responses and lead to novel therapies. Here we show that the CD4 binding human immunodeficiency virus-1 envelope glycoprotein gp120 is a useful and potent tool for functional activation of human Tregs in vitro and in vivo. Gp120 activates human Tregs by binding and signaling through CD4. Upon stimulation with gp120, human Tregs accumulate cyclic adenosine monophosphate (cAMP) in their cytosol. Inhibition of endogeneous cA…

ImmunologyTransplantation HeterologousGraft vs Host Diseasechemical and pharmacologic phenomenaCHO CellsMice SCIDBiologyHIV Envelope Protein gp120Lymphocyte ActivationBiochemistryT-Lymphocytes RegulatoryImmune tolerancechemistry.chemical_compoundMiceImmune systemCricetulusIn vivoMice Inbred NODCricetinaeCyclic AMPImmune ToleranceAnimalsHumansCyclic adenosine monophosphateIL-2 receptorhemic and immune systemsCell BiologyHematologyEnvelope glycoprotein GP120Cell biologyTransplantationchemistryImmunologyCD4 Antigensbiology.proteinHIV-1Signal transductionSignal TransductionBlood
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Increased susceptibility of complement factor B/C2 double knockout mice and mannan-binding lectin knockout mice to systemic infection with Candida al…

2008

Candida albicans is the major cause of systemic fungal infections in immunocompromised patients. We investigated the susceptibility of mice deficient in complement factor B and C2 (Bf/C2-/-), C1q (C1qa-/-), and mannan-binding lectin (MBL)-A (MBL-A) and MBL-C (MBL-A/C-/-) to systemic infection with C. albicans. Animals were infected i.p. with 10(8)C. albicans blastoconidia and monitored for mortality. Bf/C2-/- mice showed high mortality (over 90%) within the study period of 3 weeks. In contrast, mortality in C1qa-/- mice was below 15% whereas that of MBL-A/C-/- mice was 40% (P0.001). Intravenous infection of mice with 8x10(5) blastoconidia resulted in the same trend with Bf/C2-/- mice being …

Immunologychemical and pharmacologic phenomenaOpportunistic InfectionsMannose-Binding LectinBlastoconidiumComplement factor BMicrobiologyMicePhagocytosisSpecies SpecificityCandida albicansAnimalsGenetic Predisposition to DiseaseCandida albicansDouble knockoutComplement ActivationMolecular BiologyMannan-binding lectinMice KnockoutbiologyCandidiasisLectinComplement Pathway Mannose-Binding LectinComplement C2bacterial infections and mycosesbiology.organism_classificationCorpus albicansKnockout mousebiology.proteinComplement Factor BMolecular Immunology
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Synergistic Platelet Inhibitory Effect of the Phosphodiesterase Inhibitor Piroximone and Iloprost

1992

Platelet activity is regulated through synthesis and degradation of the intracellular second messengers cAMP or cGMP. The antiplatelet effect of the phosphodiesterase (PDE) III inhibitor Piroximone (PIR) was studied in vitro in platelet rich plasma. ADP induced aggregation was inhibited by PIR with an IC50 of 67 +/- 43 microM. The inhibitory effect was time and dose dependent. The antiaggregatory effects in vivo were studied in anaesthetised rats. Reduction of platelet count following injection of 100 micrograms/kg bw collagen was measured after bolus injection of PIR and vehicle. Piroximone bolus 2 mg/kg bw resulted in a 50% inhibition of platelet aggregation in rats. Cyclic AMP levels in …

In vivoChemistrymedicinePhosphodiesterasePlatelet aggregation inhibitorProstacyclinPlateletPlatelet activationPhosphodiesterase inhibitorPharmacologyIloprostmedicine.drug
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Inhibition of astroglial cell proliferation by alcohols: interference with the protein kinase C-phospholipase D signaling pathway.

2000

Abstract Ethanol inhibits astroglial cell proliferation, an effect that may contribute to the development of alcoholic embryopathy in humans. In the present study, we investigated inhibitory effects of ethanol and butanol isomers (1-, 2- and t -butanol) on astroglial cell proliferation induced by the strongly mitogenic phorbol ester, 4s-phorbol-12α,13s-dibutyrate (PDB). 4s-Phorbol-12α,13s-dibutyrate (PDB) induced a 10-fold increase of [3H]thymidine incorporation in cortical astrocytes prepared from newborn rats (EC 50 : 70 nM) which was blocked by Ro 31-8220, a cell-permeable protein kinase C (PKC) inhibitor. Ethanol blocked PDB-induced astroglial proliferation in a concentration-dependent …

IndolesButanolsPhosphatidic AcidsDiglycerideschemistry.chemical_compoundDevelopmental NeurosciencePhorbol EstersPhospholipase DAnimalsEnzyme InhibitorsProtein kinase CCells CulturedPhorbol 1213-DibutyrateProtein Kinase CEthanolEthanolCell growthPhospholipase DBrainCentral Nervous System DepressantsPhosphatidic acidequipment and suppliesIn vitroRatsEnzyme ActivationchemistryBiochemistryAstrocytesCarcinogenslipids (amino acids peptides and proteins)PhosphatidylethanolSignal transductionCell DivisionDevelopmental BiologySignal TransductionInternational journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
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Diacylglycerols containing Omega 3 and Omega 6 fatty acids bind to RasGRP and modulate MAP kinase activation.

2003

We elucidated the effects of different diacylglycerols (DAGs), i.e. 1-stearoyl-2-arachidonoyl-sn-glycerol (SAG), 1-stearoyl-2-docosahexaenoyl-sn-glycerol (SDG), and 1-stearoyl-2-eicosapentaenoyl-sn-glycerol (SEG), on [3H]PDBu binding to RasGRP. The competition studies with these DAGs on [3H]PDBu binding to RasGRP revealed different Ki values for these DAG molecular species. Furthermore, we transfected human Jurkat T cells by a plasmid containing RasGRP and assessed the implication of endogenous DAGs on activation of MAP kinases ERK1/ERK2, induced by phorbol-12-myristate-13-acetate (PMA). In control cells, GF109203X, a protein kinase C inhibitor, inhibited ERK1/ERK2 activation. However, this…

IndolesTime FactorsBiochemistryJurkat cellsMaleimideschemistry.chemical_compoundJurkat CellsGuanine Nucleotide Exchange FactorsEnzyme InhibitorsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3KinaseFatty AcidsBrainTransfectionCell biologyDNA-Binding ProteinsBiochemistryEicosapentaenoic AcidDocosahexaenoic acidMitogen-activated protein kinasePhosphorylationTetradecanoylphorbol Acetatelipids (amino acids peptides and proteins)Arachidonic acidMitogen-Activated Protein KinasesPlasmidsProtein BindingDNA ComplementaryDocosahexaenoic AcidsMAP Kinase Signaling SystemImmunoblottingBiologyTransfectionBinding CompetitiveDiglyceridesInhibitory Concentration 50Fatty Acids Omega-6Fatty Acids Omega-3Escherichia coliAnimalsHumansCalphostinMolecular BiologyDose-Response Relationship Drugurogenital systemCell BiologyRatsEnzyme ActivationKineticschemistrybiology.proteinThe Journal of biological chemistry
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HSP70 sequestration by free α-globin promotes ineffective erythropoiesis in β-thalassaemia

2014

International audience; β-Thalassaemia major (β-TM) is an inherited haemoglobinopathy caused by a quantitative defect in the synthesis of β-globin chains of haemoglobin, leading to the accumulation of free α-globin chains that form toxic aggregates. Despite extensive knowledge of the molecular defects causing β-TM, little is known of the mechanisms responsible for the ineffective erythropoiesis observed in the condition, which is characterized by accelerated erythroid differentiation, maturation arrest and apoptosis at the polychromatophilic stage. We have previously demonstrated that normal human erythroid maturation requires a transient activation of caspase-3 at the later stages of matur…

Ineffective erythropoiesisCytoplasmErythroblastsCell SurvivalMutantApoptosis[ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyalpha-globin[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Biologymedicine.disease_causeProtein Refolding03 medical and health sciences0302 clinical medicinealpha-GlobinsBone Marrowhemic and lymphatic diseasesmedicineHumans[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyErythropoiesisGATA1 Transcription FactorHSP70 Heat-Shock ProteinsMolecular Targeted TherapyCells CulturedHSP70030304 developmental biologyRegulation of gene expressionCell Nucleus0303 health sciencesMultidisciplinaryCaspase 3beta-Thalassemia[ SDV.BC.BC ] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]GATA1[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMolecular biologyHsp70Enzyme ActivationKineticsGene Expression RegulationCytoplasm030220 oncology & carcinogenesisChaperone (protein)biology.proteinErythropoiesisbeta-ThalassaemiaProtein Binding
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