Search results for "ACTIVATOR"

showing 10 items of 488 documents

Transcriptional regulation of the stem cell leukemia gene by PU.1 and Elf-1.

1998

Abstract The SCL gene, also known astal-1, encodes a basic helix-loop-helix transcription factor that is pivotal for the normal development of all hematopoietic lineages. SCL is expressed in committed erythroid, mast, and megakaryocytic cells as well as in hematopoietic stem cells. Nothing is known about the regulation of SCL transcription in mast cells, and in other lineages GATA-1 is the only tissue-specific transcription factor recognized to regulate the SCL gene. We have therefore analyzed the molecular mechanisms underlyingSCL expression in mast cells. In this paper, we demonstrate that SCL promoter 1a was regulated by GATA-1 together with Sp1 and Sp3 in a manner similar to the situati…

Transcription GeneticDNA FootprintingBiologyBiochemistryCell LineMiceTranscription (biology)hemic and lymphatic diseasesProto-Oncogene ProteinsmedicineTranscriptional regulationBasic Helix-Loop-Helix Transcription FactorsAnimalsMast CellsPromoter Regions GeneticMolecular BiologyTranscription factorT-Cell Acute Lymphocytic Leukemia Protein 1DNA PrimersBase SequenceGATA2Nuclear ProteinsGATA1Cell BiologyMast cellMolecular biologyDNA-Binding ProteinsHaematopoiesismedicine.anatomical_structureGene Expression RegulationMutagenesis Site-DirectedTrans-ActivatorsStem cellTranscription FactorsThe Journal of biological chemistry
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Promoter activity of the sea urchin (Paracentrotus lividus) nucleosomal H3 and H2A and linker H1 a-histone genes is modulated by enhancer and chromat…

2009

Core promoters and chromatin insulators are key regulatory elements that may direct a transcriptional enhancer to prefer a specific promoter in complex genetic loci. Enhancer and insulator flank the sea urchin (Paracentrotus lividus) alpha-histone H2A transcription unit in a tandem repeated cluster containing the five histone genes. This article deals with the specificity of interaction between the H2A enhancer-bound MBF-1 activator and histone gene promoters, and with the mechanism that leads the H1 transcripts to peak at about one-third of the value for nucleosomal H3 and H2A mRNAs. To this end, in vivo competition assays of enhancer and insulator functions were performed. Our evidence su…

Transcription GeneticEnhancer RNAsSettore BIO/11 - Biologia MolecolareGene Regulation Chromatin and EpigeneticsParacentrotus lividusHistonesGeneticsAnimalsNucleosomesea urchin enhancer chromatin insulator histone gene expression microinjectionTransgenesPromoter Regions GeneticEnhancerTranscription factorBinding SitesbiologyPromoterbiology.organism_classificationMolecular biologyChromatinNucleosomesChromatinEnhancer Elements GeneticHistoneembryonic structuresParacentrotusTrans-Activatorsbiology.proteinInsulator Elements
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Urokinase activates macrophage PON2 gene transcription via the PI3K/ROS/MEK/SREBP-2 signalling cascade mediated by the PDGFR-β

2009

Aims We have recently shown that urokinase plasminogen activator (uPA) increases oxidative stress (OS), cholesterol biosynthesis, and paraoxonase 2 (PON2) expression in macrophages via binding to its receptor, the uPAR. Since PON2 is regulated by both OS and cholesterol content, we hypothesized that uPA elicits a cascade of signal transduction events shared by NADPH oxidase and cholesterol biosynthesis that culminates in PON2 gene expression. Here, we investigated the signalling pathway that leads to the expression of PON2 in macrophages in response to uPA. Methods and results The increase in macrophage PON2 mRNA levels in response to uPA was shown to depend on PON2 gene promoter activation…

Transcription GeneticPhysiologyReceptor Platelet-Derived Growth Factor betaPhosphatidylinositol 3-KinasesPhysiology (medical)Gene expressionHumansExtracellular Signal-Regulated MAP KinasesTranscription factorCells CulturedMitogen-Activated Protein Kinase KinasesRegulation of gene expressionNADPH oxidasebiologyAryldialkylphosphataseKinaseMacrophagesNADPH OxidasesUrokinase-Type Plasminogen ActivatorCell biologySterol regulatory element-binding proteinUrokinase receptorGene Expression RegulationBiochemistryTissue Plasminogen Activatorbiology.proteinSignal transductionReactive Oxygen SpeciesCardiology and Cardiovascular MedicineSignal TransductionSterol Regulatory Element Binding Protein 2Cardiovascular Research
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Cross-talk between Different Enhancer Elements during Mitogenic Induction of the Human Stromelysin-1 Gene

1996

Platelet-derived growth factor (PDGF) induces the expression of human stromelysin-1, a matrix metalloproteinase involved in tumor invasion and metastasis. Here it is shown that stromelysin-1 gene induction by PDGF depends on Ras and involves three previously identified promoter elements (the stromelysin-1 PDGF-responsive element (SPRE) site, the two head-to-head polyomavirus enhancer A-binding protein-3 (PEA3) sites, and the activator protein-1 (AP-1) binding site). During mitogenic induction, these responsive elements appear to be organized in two independent transcriptional units, SPRE-AP-1 and PEA3-AP-1, which result from specific element cross-talking. Interestingly, expression of a dom…

Transcription GeneticProto-Oncogene Proteins c-junMolecular Sequence DataProtein Serine-Threonine KinasesBiologyTransfectionBiochemistryStromelysin 1Proto-Oncogene Proteins p21(ras)MiceProto-Oncogene ProteinsAnimalsHumansBinding siteEnhancerMolecular BiologyTranscription factorGeneProtein Kinase CProtein kinase CPlatelet-Derived Growth FactorBase SequenceActivator (genetics)Metalloendopeptidases3T3 CellsCell BiologyMolecular biologyRecombinant ProteinsDNA-Binding ProteinsProto-Oncogene Proteins c-rafTranscription Factor AP-1Enhancer Elements GeneticEnzyme Inductionbiology.proteinMatrix Metalloproteinase 3MitogensPlatelet-derived growth factor receptorJournal of Biological Chemistry
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Mechanism of leptin expression in breast cancer cells: role of hypoxia-inducible factor-1α

2007

We reported previously that the obesity hormone leptin is overexpressed in breast cancer biopsies. Here, we investigated molecular mechanisms involved in this process, focusing on conditions that are associated with obesity, that is, hyperinsulinemia and induction of hypoxia. By using quantitative real-time PCR, immunofluorescent detection of proteins and enzyme-linked immunosorbent assays, we found that treatment of MCF-7 breast cancer cells with high doses of insulin or the hypoxia-mimetic agent CoCl2, or culturing the cells under hypoxic conditions significantly increased the expression of leptin mRNA and protein. Notably, the greatest leptin mRNA and protein expression were observed und…

Transcriptional ActivationCancer Researchmedicine.medical_specialtyActive Transport Cell NucleusBreast NeoplasmsBiologymedicine.disease_causeleptinbreast cancerInternal medicineCoactivatorGene expressionTumor Cells CulturedGeneticsmedicineHumansInsulinHIFp300-CBP Transcription FactorsPromoter Regions GeneticMolecular BiologyCell NucleusRegulation of gene expressionBinding SitesLeptin receptorLeptinPromoterCobaltHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaGene Expression Regulation NeoplasticEndocrinologyhyperinsulinemiaCarcinogenesisChromatin immunoprecipitationhormones hormone substitutes and hormone antagonistsProtein BindingOncogene
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CD8 T Cells Control Cytomegalovirus Latency by Epitope-Specific Sensing of Transcriptional Reactivation

2006

ABSTRACT During murine cytomegalovirus (mCMV) latency in the lungs, most of the viral genomes are transcriptionally silent at the major immediate-early locus, but rare and stochastic episodes of desilencing lead to the expression of IE1 transcripts. This low-frequency but perpetual expression is accompanied by an activation of lung-resident effector-memory CD8 T cells specific for the antigenic peptide 168-YPHFMPTNL-176, which is derivedfrom the IE1 protein. These molecular and immunological findings were combined in the “silencing/desilencing and immune sensing hypothesis” of cytomegalovirus latency and reactivation. This hypothesis proposes that IE1 gene expression proceeds to cell surfac…

Transcriptional ActivationMuromegalovirusvirusesImmunologyAntigen presentationCD8-Positive T-LymphocytesVirus ReplicationMajor histocompatibility complexModels BiologicalMicrobiologyEpitopeImmediate-Early ProteinsEpitopesImmunocompromised HostMiceAntigenVirologyMHC class IVirus latencymedicineAnimalsGene silencingCytotoxic T cellAmino Acid SequenceAntigens ViralLungBone Marrow TransplantationMice Inbred BALB CBase Sequencebiologyvirus diseasesHerpesviridae Infectionsbiochemical phenomena metabolism and nutritionmedicine.diseaseVirologyMolecular biologyVirus LatencyVirus-Cell InteractionsPhenotypeAmino Acid SubstitutionInsect ScienceDNA ViralMutagenesis Site-DirectedTrans-Activatorsbiology.proteinFemaleJournal of Virology
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Reduction of Cardiac Fibrosis by Interference With YAP-Dependent Transactivation

2022

Background: Conversion of cardiac stromal cells into myofibroblasts is typically associated with hypoxia conditions, metabolic insults, and/or inflammation, all of which are predisposing factors to cardiac fibrosis and heart failure. We hypothesized that this conversion could be also mediated by response of these cells to mechanical cues through activation of the Hippo transcriptional pathway. The objective of the present study was to assess the role of cellular/nuclear straining forces acting in myofibroblast differentiation of cardiac stromal cells under the control of YAP (yes-associated protein) transcription factor and to validate this finding using a pharmacological agent that interf…

Transcriptional ActivationPhysiologyfibrosismyofibroblastsVerteporfinheart failureYAP-Signaling ProteinsSettore MED/11 - Malattie dell'Apparato CardiovascolareSettore MED/23 - Chirurgia Cardiacafibrosis; heart failure; myofibroblasts; stromal cell; transcription factorsstromal cellPhosphoproteinscell mechanics; fibrosis; heart failure; myofibroblasts; stromal cell; YAP transcription factor;MiceYAP transcription factorcell mechanicsSettore CHIM/09 - Farmaceutico Tecnologico Applicativotranscription factorsTrans-ActivatorsAnimalsHumansCardiology and Cardiovascular MedicineAdaptor Proteins Signal Transducing
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Physiological activation of the IgH 3' enhancer in B lineage cells is not blocked by Pax-5.

1996

The mouse 3' enhancer contains a high-affinity binding site for the paired box protein Pax-5. Here, we demonstrate by genomic footprinting that the rat 3' enhancer contains a low-affinity binding site for Pax-5, which is occupied in activated splenic B cells. Thus, binding of Pax-5 to the IgH 3' enhancer appears to be evolutionarily conserved in rodents. Analysis of Pax-5 expression in primary B cells demonstrates that Pax-5 remains expressed after 4 days of lipopolysaccharide (LPS) induction, but is down-regulated in 5-day stimulated cells. Similarly, the expression of Pax-5 is down-regulated in vivo in activated large splenocytes, in contrast to small resting cells. Multimerization of the…

Transcriptional Activationcongenital hereditary and neonatal diseases and abnormalitiesanimal structuresImmunologyCD40 LigandDNA FootprintingHeterologousDown-RegulationReceptors Antigen B-CellEnhancer RNAsLymphocyte ActivationMiceGene expressionImmunology and AllergyAnimalsBinding siteEnhancerTranscription factorCells CulturedReporter geneB-LymphocytesCD40Membrane GlycoproteinsbiologyGenes ImmunoglobulinPAX5 Transcription FactorNuclear ProteinsMolecular biologyRatsUp-Regulationbody regionsDNA-Binding ProteinsRepressor ProteinsEnhancer Elements GeneticGene Expression Regulationembryonic structuresbiology.proteinTrans-Activatorssense organsTranscription FactorsEuropean journal of immunology
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Synthetic retinoids dissociate coactivator binding from corepressor release.

2002

The ligand-activated retinoid receptors RXR and RAR control development, homeostasis and disease by regulating transcription of retinoic acid (RA) responsive target genes or crosstalk with other signalling pathways. According to the current model ligand-binding triggers an exchange between corepressor- and coactivator-complexes that inhibit or potentiate transcription by deacetylating and acetylating nucleosomal histones, respectively. Additional cofactors may modify the transcriptional regulatory process by linking liganded retinoid receptors to structural components of chromatin or protein degradation. The desire to specifically influence defined events in RA-signalling, while others are …

Transcriptional Activationmedicine.drug_classReceptors Retinoic AcidAmino Acid MotifsProtein degradationRetinoid X receptorBiologyLigandsBiochemistryRetinoidsCoactivatorChlorocebus aethiopsmedicineAnimalsHumansNuclear Receptor Co-Repressor 1Protein IsoformsNuclear Receptor Co-Repressor 2RetinoidMolecular BiologyNuclear receptor co-repressor 2PELP-1Binding SitesRetinoid X receptor alphaRetinoic Acid Receptor alphaNuclear ProteinsCell BiologyCell biologyDNA-Binding ProteinsRepressor ProteinsBiochemistryGene Expression RegulationCOS CellsMutagenesis Site-DirectedCorepressorHeLa CellsJournal of receptor and signal transduction research
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Switch between tyrosinase and catecholoxidase activity of scorpion hemocyanin by allosteric effectors

2008

AbstractPhenoloxidases and hemocyanins have similar type 3 copper centers although they perform different functions. Hemocyanins are oxygen carriers, while phenoloxidases (tyrosinase/catecholoxidase) catalyze the initial step in melanin synthesis. Tyrosinases catalyze two subsequent reactions, whereas catecholoxidases catalyze only the second one. Recent results indicate that hemocyanins can also function as phenoloxidases and here we show for the first time that hemocyanin can be converted to phenoloxidase. Furthermore, its substrate specificity can be switched between catecholoxidase and tyrosinase activity depending on effectors such as hydroxymethyl-aminomethan (Tris) and Mg2+-ions. Thi…

TrisStereochemistrymedicine.medical_treatmentTyrosinaseDopamineAllosteric regulationActivated hemocyaninBiophysicsMagnesium ChlorideTyramineType 3 copper proteinchemical and pharmacologic phenomenaBiochemistryCatalysisSubstrate SpecificityScorpionschemistry.chemical_compoundEnzyme activatorAllosteric RegulationStructural BiologyHemolymphHemolymphGeneticsmedicineAnimalsCatechol oxidaseMolecular BiologyScorpion Pandinus imperatorbiologyMonophenol MonooxygenaseSpectrum AnalysisActive siteCatecholoxidaseHemocyaninCell BiologyEnzyme ActivationchemistryBiochemistryHemocyaninsbiology.proteinTyrosinaseCatechol OxidaseFEBS Letters
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