Search results for "Transduction"

showing 10 items of 2149 documents

Synergistic activation of dendritic cells by combined Toll-like receptor ligation induces superior CTL responses in vivo.

2006

Toll-like receptors (TLRs) are able to interact with pathogen-derived products and their signals induce the coordinated activation of innate and adaptive immune mechanisms. Dendritic cells (DCs) play a central role in these events. As the different TLRs are able to trigger MyD88/TRIF-dependent and -independent signaling pathways, we wondered if the simultaneous activation of these signaling cascades would synergize with respect to DC activation and induce superior cytotoxic T-lymphocyte (CTL) activity in vivo. We observed that indeed the combined activation of MyD88-dependent and -independent signaling induced by TLR7 and TLR3 ligands provoked a more rapid and more sustained bone marrow–der…

T-LymphocytesImmunologyBone Marrow CellsBiologyLigandsBiochemistryT-Lymphocytes RegulatoryMiceCytotoxic T cellAnimalsAntigen-presenting cellAdaptor Proteins Signal TransducingCD86Toll-like receptorCD40Membrane GlycoproteinsToll-Like ReceptorsImmunityhemic and immune systemsCell BiologyHematologyDendritic cellDendritic CellsAcquired immune systemCell biologyToll-Like Receptor 3Mice Inbred C57BLCTL*Toll-Like Receptor 7ImmunologyMyeloid Differentiation Factor 88biology.proteinSignal TransductionT-Lymphocytes CytotoxicBlood
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NFATc1 affects mouse splenic B cell function by controlling the calcineurin–NFAT signaling network

2011

Mouse B cells lacking NFATc1 exhibit defective proliferation, survival, isotype class switching, cytokine production, and T cell help.

T-LymphocytesImmunologyNaive B cellB-cell receptorReceptors Antigen B-CellLymphocyte ActivationArticleMice03 medical and health sciences0302 clinical medicinemedicineAnimalsImmunology and AllergyB cell030304 developmental biologyB-Lymphocytes0303 health sciencesCD40NFATC Transcription Factorsintegumentary systembiologyCalcineurinCD22Germinal centerImmunoglobulin Class SwitchingMolecular biology3. Good healthB-1 cellCalcineurinmedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchbiology.proteinCalciumSpleenSignal TransductionJournal of Experimental Medicine
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Different Efficiency of Heat Shock Proteins (HSP) to Activate Human Monocytes and Dendritic Cells: Superiority of HSP60

2002

Abstract One essential immunoregulatory function of heat shock protein (HSP) is activation of the innate immune system. We investigated the activation of human monocytes and monocyte-derived dendritic cells (DC) by recombinant human HSP60, human inducible HSP72, and preparations of human gp96 and HSP70 under stringent conditions, in the absence of serum and with highly purified monocytes. HSP60 induced human DC maturation and activated human DC to secrete proinflammatory cytokines. HSP72 induced DC maturation to a lesser extent, but activated human monocytes and immature DC as efficiently as HSP60 to release proinflammatory cytokines. The independence of the effects of HSP60 and HSP72 from …

T-Lymphocytesmedicine.medical_treatmentImmunologyHSP72 Heat-Shock ProteinsPeptide bindingBiologyLymphocyte ActivationMonocytesProinflammatory cytokineAntigens NeoplasmHeat shock proteinmedicineHumansImmunology and AllergyHSP70 Heat-Shock ProteinsSecretionHeat-Shock ProteinsInnate immune systemCell DifferentiationChaperonin 60Dendritic CellsMolecular biologyCoculture TechniquesRecombinant ProteinsHsp70CytokineCytokinesHSP60Inflammation MediatorsSignal TransductionThe Journal of Immunology
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T Cells Integrate Local and Global Cues to Discriminate between Structurally Similar Antigens

2015

International audience; T lymphocytes' ability to discriminate between structurally related antigens has been attributed to the unique signaling properties of the T cell receptor. However, recent studies have suggested that the output of this discrimination process is conditioned by environmental cues. Here, we demonstrate how the IL-2 cytokine, collectively generated by strongly activated T cell clones, can induce weaker T cell clones to proliferate. We identify the PI3K pathway as being critical for integrating the antigen and cytokine responses and for controlling cell-cycle entry. We build a hybrid stochastic/deterministic computational model that accounts for such signal synergism and …

T-Lymphocytesmedicine.medical_treatmentT cellEFFECTORMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyLYMPHOCYTESArticleGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineACTIVATIONMicePhosphatidylinositol 3-KinasesAntigenmedicineAnimalsAntigenslcsh:QH301-705.5Sensory cuePI3K/AKT/mTOR pathwayAFFINITYIL-2T-cell receptorMEMORYPROLIFERATIONRECOGNITIONCell biologyMice Inbred C57BLCytokinemedicine.anatomical_structureDIFFERENTIATIONlcsh:Biology (General)ImmunologyCytokinesInterleukin-2Signal transductionTCRSignal Transduction
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Cutting Edge: A Key Pathogenic Role of IL-27 in T Cell- Mediated Hepatitis

2007

Abstract The signals driving T cell activation in T cell-mediated fulminant hepatitis are not fully understood. In this study, we identify the cytokine IL-27p28/EBI3 as a major pathogenic factor in the ConA model of T cell-mediated hepatitis. We found an up-regulation of hepatic EBI3 and p28 expression and augmented levels of IL-27 in wild-type mice after ConA administration, suggesting a potential pathogenic role of this cytokine in ConA hepatitis. Consistently, IL-27 EBI3-deficient mice were almost completely protected from ConA-induced liver damage. Such protection was associated with reduced levels of IFN-γ and its signaling proteins pSTAT-1 and T-bet. Finally, in vivo blockade of IL-27…

T-Lymphocytesmedicine.medical_treatmentT cellImmunologychemical and pharmacologic phenomenaBiologyMinor Histocompatibility AntigensInterferon-gammaMiceConcanavalin AmedicineAnimalsImmunology and AllergyReceptors CytokineReceptorFulminant hepatitisMice KnockoutHepatitisLiver injuryInterleukin-17EBI3medicine.diseaseUp-RegulationSTAT1 Transcription FactorCytokinemedicine.anatomical_structureImmunologyChemical and Drug Induced Liver InjurySignal transductionSignal TransductionThe Journal of Immunology
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A Regulatory Mechanism Involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the Control of Cell Proliferation

2011

Abstract TBP-1 /Tat-Binding Protein 1 (also named Rpt-5, S6a or PSMC3) is a multifunctional protein, originally identified as a regulator of HIV-1-Tat mediated transcription. It is an AAA-ATPase component of the 19S regulative subunit of the proteasome and, as other members of this protein family, fulfils different cellular functions including proteolysis and transcriptional regulation. We and others reported that over expression of TBP-1 diminishes cell proliferation in different cellular contexts with mechanisms yet to be defined. Accordingly, we demonstrated that TBP-1 binds to and stabilizes the p14ARF oncosuppressor increasing its anti-oncogenic functions. However, TBP-1 restrains cell…

TBP-1/Tat-Binding Protein 1lcsh:Medicinemacromolecular substancesBiologymTORC2Cell GrowthTBP-1/Tat-Binding Protein 1; cell proliferationp14arfMolecular Cell BiologyGeneticsCancer GeneticsTranscriptional regulationGene Networkslcsh:ScienceBiologyProtein kinase BPI3K/AKT/mTOR pathwayMultidisciplinaryCell growthAKTBinding proteinlcsh:RMolecular biologySignaling CascadesCell biologyTBP-1enzymes and coenzymes (carbohydrates)cell proliferationbiology.proteinMdm2lcsh:QCell DivisionResearch ArticleSignal TransductionPLoS ONE
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The Activation Status of the TGF-β Transducer Smad2 Is Associated with a Reduced Survival in Gastrointestinal Cancers: A Systematic Review and Meta-A…

2019

Aberrant function of Smad2, a crucial member of transforming growth factor beta (TGF-β) signaling, is associated with the development of malignancies, particularly in the gastrointestinal district. However, little is known about its possible prognostic role in such tumor types. With the first meta-analysis on this topic, we demonstrated that the lack of the activated form of Smad2 (phosphor-Smad2 or pSmad2), which was meant to be the C-terminally phosphorylated form, showed a statistically significant association with an increased risk of all-cause mortality in patients with gastrointestinal cancers (RR, 1.58; 95% CI, 1.05–2.37, p = 0.029, I2 = 84%), also after having adjusted for potential…

TGF-β0301 basic medicineOncologymedicine.medical_specialtySmad2 ProteinReviewCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaInternal medicineOdds RatiomedicineHumansIn patientPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyGastrointestinal Neoplasmsbiologyphosphorylationbusiness.industryOrganic ChemistryConfoundingCancerGeneral MedicineTransforming growth factor betaPrognosismedicine.diseaseComputer Science Applications030104 developmental biologyIncreased risklcsh:Biology (General)lcsh:QD1-999pSmad2030220 oncology & carcinogenesisMeta-analysisbiology.proteinPhosphorylationsignalingbusinessPublication BiasBiomarkersSmad2Signal TransductionTransforming growth factorInternational Journal of Molecular Sciences
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A Transition Zone Complex Regulates Mammalian Ciliogenesis and Ciliary Membrane Composition

2011

Mutations in genes encoding ciliary components cause ciliopathies, but how many of these mutations disrupt ciliary function is unclear. We investigated Tectonic1 (Tctn1), a regulator of mouse Hedgehog signaling, and found that it is essential for ciliogenesis in some, but not all, tissues. Cell types that do not require Tctn1 for ciliogenesis require it to localize select membrane-associated proteins to the cilium, including Arl13b, AC3, Smoothened and Pkd2. Tctn1 forms a complex with multiple ciliopathy proteins associated with Meckel (MKS) and Joubert (JBTS) syndromes, including Mks1, Tmem216, Tmem67, Cep290, B9d1, Tctn2, and Cc2d2a. Components of the Tectonic ciliopathy complex colocaliz…

TMEM67Inbred C57BLCiliopathiesMedical and Health SciencesMice0302 clinical medicineCerebellumMorphogenesisEye AbnormalitiesEncephalocelePediatricMice Knockout0303 health sciencesPolycystic Kidney DiseasesCiliumCiliary transition zoneBiological SciencesKidney Diseases CysticCell biologyOrgan SpecificityCiliary Motility DisordersKidney DiseasesRabbitsAbnormalitiesMultipleRetinitis PigmentosaCiliary Motility DisordersSignal TransductionKnockoutBiologyRetinaArticle03 medical and health sciencesCysticRare DiseasesCerebellar DiseasesCiliogenesisGeneticsMatrix-Assisted Laser Desorption-IonizationAnimalsHumansAbnormalities MultipleCiliaCiliary membrane030304 developmental biologySpectrometryCell MembraneMembrane ProteinsMassPeptide FragmentsMice Inbred C57BLSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationMutationCiliary baseChickens030217 neurology & neurosurgeryDevelopmental BiologyNature genetics
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Regulation of B cell homeostasis and activation by the tumor suppressor gene CYLD

2007

B cell homeostasis is regulated by multiple signaling processes, including nuclear factor-kappaB (NF-kappaB), BAFF-, and B cell receptor signaling. Conditional disruption of genes involved in these pathways has shed light on the mechanisms governing signaling from the cell surface to the nucleus. We describe a novel mouse strain that expresses solely and excessively a naturally occurring splice variant of CYLD (CYLD(ex7/8) mice), which is a deubiquitinating enzyme that is integral to NF-kappaB signaling. This shorter CYLD protein lacks the TRAF2 and NEMO binding sites present in full-length CYLD. A dramatic expansion of mature B lymphocyte populations in all peripheral lymphoid organs occur…

TRAF2Tumor suppressor geneImmunologyCellBiologyArticleDeubiquitinating Enzyme CYLDMiceB cell homeostasismedicineAnimalsHomeostasisImmunology and AllergyB-cell activating factorEmbryonic Stem CellsSequence DeletionB-LymphocytesRELBGenetic VariationExonsArticlesFibroblastsDeubiquitinating Enzyme CYLDAlternative SplicingCysteine Endopeptidasesmedicine.anatomical_structureProtein BiosynthesisCancer researchSignal transductionSignal TransductionJournal of Experimental Medicine
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Focal DNA Copy Number Changes in Neuroblastoma Target MYCN Regulated Genes

2013

Neuroblastoma is an embryonic tumor arising from immature sympathetic nervous system cells. Recurrent genomic alterations include MYCN and ALK amplification as well as recurrent patterns of gains and losses of whole or large partial chromosome segments. A recent whole genome sequencing effort yielded no frequently recurring mutations in genes other than those affecting ALK. However, the study further stresses the importance of DNA copy number alterations in this disease, in particular for genes implicated in neuritogenesis. Here we provide additional evidence for the importance of focal DNA copy number gains and losses, which are predominantly observed in MYCN amplified tumors. A focal 5 kb…

TRANSCRIPTIONAL TARGETNeuroblastoma/geneticsPsychologie appliquéeMedizinlcsh:MedicineChromosomal DisordersNeuroblastoma0302 clinical medicineRGS Proteins/geneticsGene duplicationMolecular Cell BiologyBasic Cancer ResearchTUMOR-SUPPRESSORALK KINASElcsh:ScienceNeurological TumorsGeneticsRegulation of gene expressionOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinACTIVATING MUTATIONSMultidisciplinaryCancer Risk FactorsHomozygoteChromosomal Deletions and DuplicationsNuclear ProteinsGenomicsSciences bio-médicales et agricolesSignaling in Selected DisciplinesCANCEROncogene Proteins/geneticsGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisMedicineRNA Long NoncodingBiologieResearch ArticleSignal TransductionEXPRESSIONDNA Copy Number VariationsGenetic Causes of CancerDown-RegulationGenomicsBiologyMolecular Genetics03 medical and health sciencesGenome Analysis ToolsNeuroblastomaCell Line TumormicroRNAmedicineGeneticsCancer GeneticsHumansGene RegulationGeneneoplasmsBiology030304 developmental biologyOncogenic SignalingN-MYCTHERAPEUTIC TARGETRECEPTORMICRORNAlcsh:RBiology and Life SciencesChromosomeCancers and NeoplasmsHuman Geneticsmedicine.diseaseNuclear Proteins/geneticsMicroRNAs/geneticsMicroRNAsPediatric Oncologylcsh:QGenome Expression AnalysisN-MycRGS ProteinsPLoS ONE
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