Search results for "down-regulation"

showing 10 items of 310 documents

Topotecan triggers apoptosis in p53-deficient cells by forcing degradation of XIAP and survivin thereby activating caspase-3-mediated Bid cleavage.

2009

The topoisomerase I inhibitor topotecan (TPT) is used in the therapy of different tumors including high-grade gliomas. We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I. Here, we show that p53-deficient (p53(-/-)) fibroblasts undergo excessive mitochondrial apoptosis featuring H2AX phosphorylation, Bcl-x(L) decline, cytochrome c release, caspase-9/-3/-2 activation, and cleavage of Bid. In wt and apaf-1(-/-) cells, caspase-2 did not become activated and Bid was not cleaved. In addition, p53(-/-) cells cotreated with TPT and caspase-3 inhibitor showed neither caspase-2 acti…

SurvivinBlotting WesternDown-RegulationCaspase 3ApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyTopoisomerase-I InhibitorInhibitor of apoptosisTransfectionInhibitor of Apoptosis ProteinsHistonesMiceCell Line TumorSurvivinAnimalsHumansPhosphorylationRNA Small InterferingPharmacologyMice KnockoutCaspase 3Caspase 2TransfectionFibroblastsFlow CytometryMolecular biologyXIAPMice Inbred C57BLRepressor ProteinsApoptotic Protease-Activating Factor 1ApoptosisCancer researchMolecular MedicineApoptosomeTopoisomerase I InhibitorsTumor Suppressor Protein p53TopotecanMicrotubule-Associated ProteinsBH3 Interacting Domain Death Agonist ProteinThe Journal of pharmacology and experimental therapeutics
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Cortical neurons selectively inhibit MHC class II induction in astrocytes but not in microglial cells.

1993

Astrocytes have been shown to act as potent accessory cells for MHC class II-restricted T cell responses in vitro after treatment with interferon-gamma. In contrast, even under conditions of severe central nervous system (CNS) inflammation, they seem to express little, if any, class II molecules in vivo. Thus the role of astroglial cells as accessory cells in immune responses in the CNS remains to be determined. We have studied neuron--glia interactions with respect to induction of MHC class II molecules. Surprisingly, in a co-culture system, viable neurons inhibited the induction of class II restriction elements on astrocytes. This effect was only observed when neurons had contact to astro…

T cellT-LymphocytesImmunologyAntigen presentationAntigen-Presenting CellsDown-RegulationLymphocyte ActivationMHC class ImedicineImmunology and AllergyAnimalsCells CulturedCerebral CortexNeuronsMHC class IIbiologyMicrogliaHistocompatibility Antigens Class IIGeneral MedicineCell biologyRatsmedicine.anatomical_structurenervous systemAstrocytesImmunologybiology.proteinNeurogliaNeuronNeurogliaAstrocyteInternational immunology
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Cutting Edge: IL-23 Cross-Regulates IL-12 Production in T Cell-Dependent Experimental Colitis

2006

Abstract Although IL-12 and IL-23 share the common p40 subunit, IL-23, rather than IL-12, seems to drive the pathogenesis of experimental autoimmune encephalomyelitis and arthritis, because IL-23/p19 knockout mice are protected from disease. In contrast, we describe in this study that newly created LacZ knockin mice deficient for IL-23 p19 were highly susceptible for the development of experimental T cell-mediated TNBS colitis and showed even more severe colitis than wild-type mice by endoscopic and histologic criteria. Subsequent studies revealed that dendritic cells from p19-deficient mice produce elevated levels of IL-12, and that IL-23 down-regulates IL-12 expression upon TLR ligation. …

T-LymphocytesTransgeneT cellImmunologyDown-RegulationMice TransgenicInterleukin-23PathogenesisMiceInterleukin 23AnimalsImmunology and AllergyMedicineColitisCells Culturedbusiness.industryInterleukinsExperimental autoimmune encephalomyelitisColitismedicine.diseaseInterleukin-12Survival RateDisease Models AnimalProtein Subunitsmedicine.anatomical_structureImmunologyKnockout mouseInterleukin-23 Subunit p19Interleukin 12Disease SusceptibilitybusinessThe Journal of Immunology
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cIAP1-dependent TRAF2 degradation regulates the differentiation of monocytes into macrophages and their response to CD40 ligand.

2008

AbstractPeripheral blood monocytes are plastic cells that migrate to tissues and differentiate into various cell types, including macrophages, dendritic cells, and osteoclasts. We have described the migration of cellular inhibitor of apoptosis protein 1 (cIAP1), a member of the IAP family of proteins, from the nucleus to the Golgi apparatus in monocytes undergoing differentiation into macrophages. Here we show that, once in the cytoplasm, cIAP1 is involved in the degradation of the adaptor protein tumor necrosis factor receptor–associated factor 2 (TRAF2) by the proteosomal machinery. Inhibition of cIAP1 prevents the decrease in TRAF2 expression that characterizes macrophage formation. We d…

TRAF2CytoplasmCellular differentiationImmunologyCD40 LigandDown-RegulationGene ExpressionGolgi ApparatusBiologyBiochemistryMonocytesProinflammatory cytokineInhibitor of Apoptosis ProteinsPhagocytes Granulocytes and MyelopoiesisPhagocytosisMacrophageHumansRNA Small InterferingCD40U937 cellMacrophagesSignal transducing adaptor proteinCell DifferentiationCell BiologyHematologyU937 CellsTNF Receptor-Associated Factor 2Molecular biologyCell biologybiology.proteinTumor necrosis factor alphaBlood
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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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Differential evolution of PSA-NCAM expression during aging of the rat telencephalon

2007

Changes in the ability of neuronal networks to undergo structural remodeling may be involved in the age-associated cognitive decline. The polysialylated form of the neural cell adhesion molecule (PSA-NCAM) declines dramatically during postnatal development, but persists in several regions of the young-adult rat telencephalon, where it participates, through its anti-adhesive properties, in neuronal structural plasticity. However, PSA-NCAM expression during aging has only been studied in the dentate gyrus and the piriform cortex layer II, where it is strongly downregulated in adult (middle-aged) individuals. Using immunohistochemistry, we have observed that in most of the telencephalic areas …

TelencephalonAgingDendritic SpinesDown-RegulationHippocampusCell CountNeural Cell Adhesion Molecule L1BiologyPiriform cortexCell AdhesionLimbic SystemmedicineNeuropilAnimalsCognitive declineCerebral CortexNeuronsNeuronal PlasticityNeocortexGeneral NeuroscienceDentate gyrusAmygdalaImmunohistochemistryRats Inbred F344RatsDisease Models Animalmedicine.anatomical_structurenervous systemSialic AcidsFemaleNeural cell adhesion moleculeNeurology (clinical)Geriatrics and GerontologyNeuroscienceBiomarkersDevelopmental BiologyStratum lucidumNeurobiology of Aging
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A homolog of the putative tumor suppressor QM in the sponge Suberites domuncula: downregulation during the transition from immortal to mortal (apopto…

1999

Abstract The activation of components of the transcription factors such as AP-1 or c-jun is essential for a physiological response of metazoan cells during aging. The activity of such proto-oncoproteins is under enzymatic control. The function of c-jun is additionally modulated by the QM protein. Here, we studied the expression of the gene, encoding the QM-like protein in the sponge Suberites domuncula . These animals contain high levels of telomerase in their somatic cells. To understand the switch from telomerase-positive immortal cells to telomerase-negative mortal cells which undergo apoptosis, the expression of the QM-like gene was measured in this system. The cDNA, termed QMSD , encod…

TelomeraseMolecular Sequence DataDown-RegulationGene ExpressionApoptosisDownregulation and upregulationComplementary DNAAnimalsHumansAmino Acid SequenceRNA MessengerCloning MolecularTranscription factorGenePhylogenyBase Sequencebiologyc-junProteinsRNA-Binding ProteinsCell BiologyGeneral Medicinebiology.organism_classificationMolecular biologyPoriferaSuberites domunculaOpen reading frameProtein BiosynthesisCarrier ProteinsDevelopmental BiologyTissue and Cell
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Activation of classical protein kinase C reduces the expression of human cationic amino acid transporter 3 (hCAT-3) in the plasma membrane

2005

We have previously shown that activation of PKC (protein kinase C) results in internalization of hCAT-1 [human CAT-1 (cationic amino acid transporter 1)] and a decrease in arginine transport [Rotmann, Strand, Martiné and Closs (2004) J. Biol. Chem. 279, 54185–54192]. However, others found increased transport rates for arginine in response to PKC activation, suggesting a differential effect of PKC on different CAT isoforms. Therefore we investigated the effect of PKC on hCAT-3, an isoform expressed in thymus, brain, ovary, uterus and mammary gland. In Xenopus laevis oocytes and human U373MG glioblastoma cells, hCAT-3-mediated L-arginine transport was significantly reduced upon treatment with…

TeratocarcinomaArginineXenopusDown-RegulationArginineBiochemistryEnzyme activatorAntibody SpecificityCell Line TumorTumor Cells CulturedAnimalsHumansMolecular BiologyProtein Kinase CProtein kinase CCationic Amino Acid Transporter 1Arginine transportbiologyActivator (genetics)Cell MembraneBiological TransportCell BiologyFusion proteinEnzyme ActivationBiochemistryTetradecanoylphorbol AcetateOocytesbiology.proteinTetradecanoylphorbol AcetateCATIONIC AMINO ACID TRANSPORTER 3GlioblastomaResearch ArticleBiochemical Journal
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The aryl hydrocarbon receptor modulates acute and late mast cell responses.

2012

Abstract The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activity is modulated by xenobiotics as well as physiological ligands. These compounds may modulate inflammatory responses and contribute to the rising prevalence of allergic diseases observed in industrialized countries. Mast cells (MCs), located within tissues at the boundary of the external environment, represent a potential target of AhR ligands. In this study, we report that murine and human MCs constitutively express AhR, and its activation by the high-affinity ligand 6-formylindolo[3,2-b]carbazole (FICZ) determines a boost in degranulation. On the contrary, repeated exposure to FICZ inhibits…

Time FactorsInbred C57BLLigandsCell DegranulationPathogenesischemistry.chemical_compoundMiceAnaphylaxiReceptorsMast CellImmunology and AllergyMast CellsReceptorMice KnockoutbiologyInterleukin-17DegranulationMast cellUp-RegulationImmunology Mast Cell Aryl Receptormedicine.anatomical_structureAryl HydrocarbonBone Marrow Celldeficiency/metabolism/physiologyIgEmedicine.symptomimmunology/metabolism/pathologyHistamineHumanReceptorTime FactorKnockoutImmunologyDown-RegulationLigandInflammationBone Marrow CellsSettore MED/08 - Anatomia PatologicaCell LinebiosynthesiAnaphylaxis; immunology/metabolism/pathology Animals Bone Marrow Cells; immunology/metabolism/pathology Cell Degranulation; genetics/immunology Cell Line Down-Regulation; genetics/immunology Humans Interleukin-17; biosynthesis Interleukin-6; biosynthesis Ligands Mast Cells; immunology/metabolism/pathology Mice Mice; Inbred C57BL Mice; Knockout Receptors; Aryl Hydrocarbon; deficiency/metabolism/physiology Receptors; IgE; physiology Time Factors Up-Regulation; genetics/immunologymedicineAnimalsHumansTranscription factorAnaphylaxisAnimalInterleukin-6Receptors IgEAryl hydrocarbon receptorgenetics/immunologyMice Inbred C57BLMAST CELL; ARYL HYDROCARBON RECEPTORchemistryReceptors Aryl HydrocarbonImmunologyphysiologybiology.proteinbiosynthesisJournal of immunology (Baltimore, Md. : 1950)
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Paclitaxel and beta-lapachone synergistically induce apoptosis in human retinoblastoma Y79 cells by downregulating the levels of phospho-Akt.

2009

Paclitaxel (PTX) and beta-lapachone (LPC) are naturally occurring compounds that have shown a large spectrum of anticancer activity. In this article we show for the first time that PTX/LPC combination induces potent synergistic apoptotic effects in human retinoblastoma Y79 cells. Combination of suboptimal doses of PTX (0.3 nM) and LPC (1.5 microM) caused biochemical and morphological signs of apoptosis at 48 h of treatment. These effects were accompanied by potent lowering in inhibitor of apoptosis proteins and by activation of Bid and caspases 3 and 6 with lamin B and PARP breakdown. PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM…

Time FactorsPhysiologyClinical BiochemistryApoptosisInhibitor of Apoptosis ProteinsWortmanninchemistry.chemical_compoundSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsPhosphorylationCaspasebiologyCaspase 6Lamin Type BCaspase 3Protein StabilityRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2TransfectionBiochemistrylipids (amino acids peptides and proteins)Poly(ADP-ribose) PolymerasesWortmanninBH3 Interacting Domain Death Agonist Proteinretinoblastoma survival factors apoptosisPaclitaxelCell SurvivalPoly ADP ribose polymeraseActive Transport Cell NucleusDown-RegulationInhibitor of apoptosisTransfectionCell Line TumorHumansProtein kinase BProtein Kinase InhibitorsCell NucleusDose-Response Relationship DrugCell BiologyAntineoplastic Agents PhytogenicAndrostadieneschemistryCell cultureApoptosisbiology.proteinCancer researchTumor Suppressor Protein p53Proto-Oncogene Proteins c-aktNaphthoquinonesJournal of cellular physiology
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