Search results for "down-regulation"

showing 10 items of 310 documents

Bovine seminal ribonuclease is cytotoxic for both malignant and normal telomerase-positive cells

2005

Bovine seminal-ribonuclease (BS-RNase) is a member of the 'ribonucleases with special biological actions' family since it possesses specific anti-tumour, anti-spermatogenic and embryotoxic activities and exerts an immunosuppressive effect on T lymphocytes. In previous studies it was demonstrated that BS-RNase induced apoptosis in proliferating, malignant and normal cells and that telomerase activity loss also caused apoptotic death in neoplastic cells. Since an obvious relationship between cell proliferation and telomerase activity exists, the aim of this work was to study if the pro-apoptotic cytotoxic action exerted by BS-RNase on proliferating malignant cells (HT29) and proliferating nor…

Cancer ResearchTelomeraseTime FactorsT-LymphocytesCellular differentiationCytotoxicityBlotting WesternDown-RegulationTetrazolium SaltsAntineoplastic AgentsApoptosisEnzyme-Linked Immunosorbent AssayBiologyHT29 CellsCell Line TumorEndoribonucleasesAnimalsHumansCytotoxic T cellTelomerase reverse transcriptaseLymphocytesRNA MessengerTelomeraseBovine seminal-ribonuclease; Cytotoxicity; HTR; Nucleolar localization; TelomeraseCell ProliferationReverse Transcriptase Polymerase Chain ReactionCell growthCell DifferentiationCell cycleNucleolar localizationMolecular biologyThiazolesBovine seminal-ribonucleaseMicroscopy FluorescenceOncologyCell cultureLeukocytes MononuclearMicroscopy Electron ScanningRNACattleHTRCell NucleolusImmunosuppressive Agents
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Suppressing an Anti-Inflammatory Cytokine Reveals a Strong Age-Dependent Survival Cost in Mice

2010

7 pages; International audience; BACKGROUND: The central paradigm of ecological immunology postulates that selection acts on immunity as to minimize its cost/benefit ratio. Costs of immunity may arise because the energetic requirements of the immune response divert resources that are no longer available for other vital functions. In addition to these resource-based costs, mis-directed or over-reacting immune responses can be particularly harmful for the host. In spite of the potential importance of immunopathology, most studies dealing with the evolution of the immune response have neglected such non resource-based costs. To keep the immune response under control, hosts have evolved regulat…

Male0106 biological sciencesSurvivalmedicine.medical_treatmentAnti-Inflammatory AgentsImmunology/ImmunomodulationDown-Regulationlcsh:MedicineInflammationBiology[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunology010603 evolutionary biology01 natural sciencesAntibodiesMice03 medical and health sciencesImmune systemImmunityImmunopathologymedicineAnimalsReceptors Interleukin-10lcsh:ScienceReceptor030304 developmental biologyInflammationEvolutionary Biology[ SDE.BE ] Environmental Sciences/Biodiversity and Ecology0303 health sciencesMultidisciplinarylcsh:RAge FactorsInterleukin-103. Good healthMice Inbred C57BLInterleukin 10CytokineEcology/Physiological Ecology[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyImmunologybiology.proteinlcsh:Q[SDE.BE]Environmental Sciences/Biodiversity and Ecologymedicine.symptomAntibodyResearch ArticlePLoS ONE
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Hypoxia and Human Genome Stability: Downregulation of BRCA2 Expression in Breast Cancer Cell Lines

2013

Previously, it has been reported that hypoxia causes increased mutagenesis and alteration in DNA repair mechanisms. In 2005, an interesting study showed that hypoxia-induced decreases in BRCA1 expression and the consequent suppression of homologous recombination may lead to genetic instability. However, nothing is yet known about the involvement of BRCA2 in hypoxic conditions in breast cancer. Initially, a cell proliferation assay allowed us to hypothesize that hypoxia could negatively regulate the breast cancer cell growth in short term in vitro studies. Subsequently, we analyzed gene expression in breast cancer cell lines exposed to hypoxic condition by microarray analysis. Interestingly,…

Genome instabilityDNA RepairArticle SubjectDNA repairDNA damageSettore MED/06 - Oncologia MedicaDown-Regulationlcsh:MedicineBreast NeoplasmsBiologyGeneral Biochemistry Genetics and Molecular BiologyGenomic InstabilityBreast cancerCell Line TumorBreast CancermedicineHumansEnzyme Inhibitorsskin and connective tissue diseasesHypoxiaBiologyGeneral Immunology and MicrobiologyBRCA1 ProteinGenome Humanlcsh:RGenome StabilityGeneral MedicineDNA repair protein XRCC4medicine.diseaseBRCA2Cell HypoxiaAmino Acids DicarboxylicGene Expression Regulation NeoplasticCancer researchDNA mismatch repairFemaleHuman medicineHypoxia; Genome Stability; BRCA2; Breast CancerHomologous recombinationEngineering sciences. TechnologyNucleotide excision repairResearch ArticleDNA Damage
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Constitutive Promoter Occupancy by the MBF-1 Activator and Chromatin Modification of the Developmental Regulated Sea Urchin α-H2A Histone Gene

2007

The tandemly repeated sea urchin alpha-histone genes are developmentally regulated. These genes are transcribed up to the early blastula stage and permanently silenced as the embryos approach gastrulation. As previously described, expression of the alpha-H2A gene depends on the binding of the MBF-1 activator to the 5' enhancer, while down-regulation relies on the functional interaction between the 3' sns 5 insulator and the GA repeats located upstream of the enhancer. As persistent MBF-1 binding and enhancer activity are detected in gastrula embryos, we have studied the molecular mechanisms that prevent the bound MBF-1 from trans-activating the H2A promoter at this stage of development. Her…

Embryo Nonmammaliananimal structuresRestriction MappingMBF-1Down-RegulationEnhancer RNAschromatin immunoprecipitationBiologyHistone DeacetylasesactivatorHistonesHistone H3Histone H1Structural BiologyHistone H2AHistone methylationAnimalsNucleosomeHistone codenucleosome phasingPromoter Regions GeneticEnhancerBase PairingMolecular Biologyhistone modificationsGene Expression Regulation DevelopmentalGastrulaMolecular biologyChromatinNucleosomesRepressor ProteinsMutagenesis InsertionalEnhancer Elements GeneticSea Urchinsembryonic structuresTrans-ActivatorsCalmodulin-Binding ProteinsInsulator Elementssea urchin histone geneProtein Processing Post-TranslationalProtein BindingJournal of Molecular Biology
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Effect of retinoids on UDP-glucuronosyltransferase 2B7 mRNA expression in Caco-2 cells.

2008

Human UDP-glucuronosyltransferase 2B7 (UGT2B7) is one of the major isoforms involved in the glucuronidation of endogenous compounds and xenobiotics. This isoform is the only human UGT shown to glucuronidate retinoids and their oxidized derivatives. In this study, the effects of all-trans retinoic acid (atRA), 9-cis RA, and the RAR agonist TTNPB, on UGT2B7 and UGT2B15 mRNA expression in Caco-2 cells have been examined. Each of these retinoids significantly suppressed UGT2B7 mRNA expression in a concentration-dependent manner with IC50 values of 3.5, 0.3, and 0.2 microM, respectively. However, no inhibition was observed when two other UGTs, UGT2B15 or -1A6, were exposed to atRA, 9-cis RA, or …

Gene isoformGlucuronosyltransferasemedicine.drug_classCell SurvivalGlucuronidationRetinoic acidPharmaceutical ScienceDown-RegulationTretinoinBenzoatesArticle03 medical and health scienceschemistry.chemical_compoundRetinoids0302 clinical medicineTretinoinmedicineHumansPharmacology (medical)RetinoidRNA MessengerGlucuronosyltransferaseAlitretinoinCells Cultured030304 developmental biologyPharmacology0303 health sciencesbiologyBiological activityUGT2B7Biochemistrychemistry030220 oncology & carcinogenesisbiology.proteinCaco-2 Cellsmedicine.drugDrug metabolism and pharmacokinetics
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Differentiation and characterization of rat adipose tissue mesenchymal stem cells into endothelial-like cells

2018

In this study, mesenchymal stem cells were isolated from rat adipose tissue (AD-MSCs) to characterize and differentiate them into endothelial-like cells. AD-MSCs were isolated by mechanical and enzymatic treatments, and their identity was verified by colony-forming units (CFU) test and by differentiation into cells of mesodermal lineages. The endothelial differentiation was induced by plating another aliquot of cells in EGM-2 medium, enriched with specific endothelial growth factors. Five subcultures were performed. The expression of stemness genes (OCT4, SOX2 and NANOG) was investigated. The presence of CD90 and the absence of the CD45 were evaluated by flow cytometry. The endothelial-like…

0301 basic medicineCellular differentiationSettore VET/09 - Clinica Chirurgica VeterinariaSettore BIO/13 - Biologia Applicataimmunophenotypical analysiCell DifferentiationNanog Homeobox ProteinGeneral MedicineCadherinsFlow CytometryUp-RegulationPlatelet Endothelial Cell Adhesion Molecule-1Endothelial stem cellDrug CombinationsAdipose Tissueembryonic structuresVeterinary (all)ProteoglycansCollagenStem cellHomeobox protein NANOGadipose-derived mesenchymal stem cellDown-RegulationCD146 AntigenBiology03 medical and health sciencesMatrigel assaySOX2Antigens CDAdipose-derived mesenchymal stem cellsAnimalsEndothelial cells differentiationRats WistarImmunophenotypical analysisMatrigelGeneral VeterinaryGene Expression ProfilingSOXB1 Transcription FactorsMesenchymal stem cellEndothelial CellsMesenchymal Stem Cells3T3-L1Molecular biologyAdipose-derived mesenchymal stem cells; Endothelial cells differentiation; Gene expression; Immunophenotypical analysis; Matrigel assay; Rat; Veterinary (all)Culture MediaRats030104 developmental biologyadipose-derived mesenchymal stem cells; endothelial cells differentiation; gene expression; immunophenotypical analysis; matrigel assay; ratLeukocyte Common AntigensThy-1 AntigensRatLamininGene expressionOctamer Transcription Factor-3
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Activation of protein kinase C alpha and/or epsilon enhances transcription of the human endothelial nitric oxide synthase gene.

1998

In primary human umbilical vein endothelial cells (HUVECs), incubation with phorbol-12-myristate-13-acetate (PMA) enhanced basal and bradykinin-stimulated nitric oxide production. In the HUVEC-derived cell line EA.hy 926, PMA and phorbol-12,13-dibutyrate stimulated endothelial nitric oxide synthase (NOS III) mRNA expression in a concentration- and time-dependent manner. Maximal mRNA expression (3.3-fold increase) was observed after 18 hr. NOS III protein and activity were increased to a similar extent. The specific protein kinase C (PKC) inhibitors bisindolylmaleimide I (1 microM), Gö 6976 [12-(2 cyanoethyl)-6,7,12, 13-tetrahydro-13-methyl-5-oxo-5H-indolo[2,3-a]pyrrolo-[3, 4-c]carbazole] (1…

Umbilical VeinsProtein Kinase C-alphaTime FactorsEndotheliumTranscription GeneticDown-RegulationProtein Kinase C-epsilonBiologyBradykininTransfectionNitric oxidechemistry.chemical_compoundEnzyme StabilitymedicineHumansRNA MessengerEnzyme InhibitorsProtein kinase APromoter Regions GeneticCyclic GMPProtein kinase CCells CulturedProtein Kinase CPharmacologyKinaseMethane sulfonateBiological TransportMolecular biologyUp-RegulationEnzyme ActivationIsoenzymesmedicine.anatomical_structureChelerythrinechemistryGene Expression RegulationCell cultureMolecular MedicineTetradecanoylphorbol AcetateEndothelium VascularNitric Oxide SynthaseMolecular pharmacology
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The Odd Sibling: Features ofβ3-Adrenoceptor Pharmacology

2014

beta(3)-Adrenoceptor agonists have recently been introduced for the treatment of overactive urinary bladder syndrome. Their target, the beta(3)-adrenoceptor, was discovered much later than beta(1)- and beta(2)-adrenoceptors and exhibits unique properties which make extrapolation of findings from the other two subtypes difficult and the beta(3)-adrenoceptor a less-understood subtype. This article discusses three aspects of beta(3)-adrenoceptor pharmacology. First, the ligand-recognition profile of beta(3)-adrenoceptors differs considerably from that of the other two subtypes, i.e., many antagonists considered as nonselective actually are beta(3)-sparing, including propranolol or nadolol. Man…

HUMAN BETA-3-ADRENERGIC RECEPTORDOWN-REGULATIONCell typemedicine.medical_specialtyADRENERGIC-RECEPTORMOUSE BETA(3)-ADRENOCEPTORAdrenergic receptormedicine.medical_treatmentSIGNAL-TRANSDUCTIONAdrenergic beta-3 Receptor AgonistsPropranololPharmacologyBiologyLigandsDownregulation and upregulationInternal medicinemedicineAnimalsHumansMOLECULAR CHARACTERIZATIONReceptorBETA-ADRENOCEPTOR AGONISTSDesensitization (medicine)PharmacologyMessenger RNABinding SitesPolymorphism GeneticOVERACTIVE BLADDEREndocrinologyGene Expression RegulationReceptors Adrenergic beta-3Molecular MedicineAdrenergic beta-3 Receptor AntagonistsSignal transductionURINARY-BLADDERMESSENGER-RNAmedicine.drugMolecular Pharmacology
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Gatekeeper of pluripotency: A common Oct4 transcriptional network operates in mouse eggs and embryonic stem cells

2011

Abstract Background Oct4 is a key factor of an expanded transcriptional network (Oct4-TN) that governs pluripotency and self-renewal in embryonic stem cells (ESCs) and in the inner cell mass from which ESCs are derived. A pending question is whether the establishment of the Oct4-TN initiates during oogenesis or after fertilisation. To this regard, recent evidence has shown that Oct4 controls a poorly known Oct4-TN central to the acquisition of the mouse egg developmental competence. The aim of this study was to investigate the identity and extension of this maternal Oct4-TN, as much as whether its presence is circumscribed to the egg or maintained beyond fertilisation. Results By comparing …

Octamer Transcription Factor-3lcsh:QH426-470lcsh:BiotechnologycellsGene regulatory networkDown-RegulationBiologyTranscriptomeMicelcsh:TP248.13-248.65GeneticsInner cell massAnimalsGene Regulatory NetworksEmbryonic Stem Cellsreproductive and urinary physiologyOligonucleotide Array Sequence AnalysisGeneticsGene Expression ProfilingfungiEmbryoEmbryonic stem cellGene expression profilinglcsh:GeneticsMultigene FamilyCancer cellembryonic structuresOocytesFemalebiological phenomena cell phenomena and immunityFunction and Dysfunction of the Nervous SystemOctamer Transcription Factor-3Research ArticleBiotechnologyBMC Genomics
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p53-Mediated downregulation of H ferritin promoter transcriptional efficiency via NF-Y.

2008

The tumor suppressor protein p53 triggers many of the cellular responses to DNA damage by regulating the transcription of a series of downstream target genes. p53 acts on the promoter of the target genes by interacting with the trimeric transcription factor NF-Y. H ferritin promoter activity is tightly dependent on a multiprotein complex called Bbf; on this complex NF-Y plays a major role. The aim of this work was to study the modulation of H ferritin expression levels by p53. CAT reporter assays indicate that: (i) p53 overexpression strongly downregulates the transcriptional efficiency driven by an H ferritin promoter construct containing only the NF-Y recognition sequence and that the phe…

Chromatin ImmunoprecipitationMultiprotein complexTranscription GeneticDown-RegulationBiologyBiochemistryTranscriptional regulationDownregulation and upregulationTranscription (biology)Transcriptional regulationFerritin geneHumansElectrophoretic mobility shift assayp300-CBP Transcription FactorsPromoter Regions GeneticTranscription factorGeneFerritin gene; Transcriptional regulation; Transcriptional factorCell BiologyHCT116 CellsMolecular biologyGene Expression Regulation NeoplasticCCAAT-Binding FactorDoxorubicinTranscriptional factorApoferritinsTumor Suppressor Protein p53Chromatin immunoprecipitationHeLa CellsProtein Binding
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