Search results for "Transcriptional Activation"

showing 10 items of 102 documents

Impairing Otp homeodomain function in oral ectoderm cells affects skeletogenesis in sea urchin embryos

2003

AbstractIn the sea urchin embryo skeletogenesis is the result of a complex series of molecular and cellular events that coordinate the morphogenetic process. Past and recent evidence strongly indicate that skeletal initiation and growth are strictly dependent on signals emanating from the oral ectodermal wall. As previously suggested, Orthopedia (Otp), a homeodomain-containing transcription factor specifically expressed in a small subset of oral ectoderm cells, might be implicated in this signalling pathway. In this study, we utilize three different strategies to address the issue of whether Otp is an upstream regulator of sketelogenesis. We describe the effects of microinjection of Otp mor…

Transcriptional Activationanimal structuresMorpholinoOrthopedia homeoboxMolecular Sequence DataEctodermNerve Tissue ProteinsBiologyFusion geneEctodermmedicineSkeletogenesisAnimalsAmino Acid SequenceSea urchin embryoTranscription factorMolecular BiologyMessenger RNAExtracellular Matrix ProteinsBone DevelopmentEmbryoCell BiologyMolecular biologyHedgehog signaling pathwayMorpholino oligonucleotidesCytoskeletal Proteinsmedicine.anatomical_structureProtein BiosynthesisSea Urchinsembryonic structuresHomeoboxDevelopmental BiologyDevelopmental Biology
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Cadmium as a transcriptional modulator in human cells

2010

Cadmium (Cd) is an underground mineral widely used in the steel industry, in plastics, and as a component of batteries. It is an industrial and environmental pollutant released as an air contaminant from fertilizers and, more prominently, in the form of wastewater. Food, drinking water, and, mainly, inhalation of smoke from cigarettes are sources of daily exposure of humans to the heavy metal. Although Cd has no known useful function for humans as well as other organisms, it appears to evoke in cells a number of responses that involve not only death signaling but also protective reactions against the toxicity. This finding prompted a number of experimental studies aimed to elucidate the cel…

Transcriptional Activationchemistry.chemical_elementApoptosisBiologyToxicologyTranscriptional regulationHumansSettore BIO/06 - Anatomia Comparata E CitologiaGeneHeat-Shock ProteinsRegulation of gene expressionPollutantCadmiumhuman cellBiochemistrychemistryGene Expression RegulationToxicityHeme Oxygenase (Decyclizing)gene expressionEnvironmental PollutantsMetallothioneinSignal transductionFunction (biology)Water Pollutants ChemicalSignal TransductionCadmium
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The Wilms' tumor suppressor gene (wt1) product regulates Dax-1 gene expression during gonadal differentiation.

1999

Gonadal differentiation is dependent upon a molecular cascade responsible for ovarian or testicular development from the bipotential gonadal ridge. Genetic analysis has implicated a number of gene products essential for this process, which include Sry, WT1, SF-1, and DAX-1. We have sought to better define the role of WT1 in this process by identifying downstream targets of WT1 during normal gonadal development. We have noticed that in the developing murine gonadal ridge, wt1 expression precedes expression of Dax-1, a nuclear receptor gene. We document here that the spatial distribution profiles of both proteins in the developing gonad overlap. We also demonstrate that WT1 can activate the D…

Transcriptional Activationcongenital hereditary and neonatal diseases and abnormalitiesGenes Wilms TumorReceptors Retinoic AcidTATA boxMolecular Sequence DataMutagenesis (molecular biology technique)Biologyurologic and male genital diseasesResponse ElementsTransactivationMiceGene expressionAnimalsHumansGonadsPromoter Regions GeneticWT1 ProteinsMolecular BiologyGeneCell Growth and DevelopmentCell Line TransformedGonadal ridgeBase Sequenceurogenital systemDAX-1 Orphan Nuclear ReceptorfungiGene Expression Regulation DevelopmentalCell Biologyfemale genital diseases and pregnancy complicationsCell biologyDNA-Binding ProteinsRepressor ProteinsTestis determining factorNuclear receptorCOS CellsCancer researchTranscription FactorsMolecular and cellular biology
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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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A differential role of CREB phosphorylation in cAMP-inducible gene expression in the rat pineal

2000

In the rat pineal gland cAMP mediates nocturnal induction of the enzyme arylalkylamine N-acetyltransferase (AA-NAT) as well as of transcription factors such as inducible cAMP early repressor (ICER), Fos-related antigen-2 (Fra-2) and JunB. Cyclic AMP stimulates the phosphorylation of the DNA binding protein cAMP response element binding protein (CREB). While cAMP-induced CREB phosphorylation appears to be a prerequisite for AA-NAT and ICER gene expression, it is not known whether CREB phosphorylation accounts for the full cAMP response of the two genes. Furthermore, the significance of CREB phosphorylation in cAMP-activated Fra-2 and JunB transcription is unknown. In the present in vitro stu…

Transcriptional Activationendocrine systemCAMP-Responsive Element ModulatorArylamine N-AcetyltransferaseProto-Oncogene Proteins c-junJUNBBlotting WesternNerve Tissue ProteinsFos-Related Antigen-2CREBPineal GlandGene Expression Regulation EnzymologicCyclic AMP Response Element ModulatorRats Sprague-DawleyOkadaic AcidGene expressionAnimalsRNA MessengerEnzyme InhibitorsPhosphorylationCyclic AMP Response Element-Binding ProteineducationMolecular BiologyTranscription factorRegulation of gene expressioneducation.field_of_studybiologyReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceMolecular biologyRatsDNA-Binding ProteinsRepressor ProteinsBucladesinebiology.proteinPhosphorylationNeurology (clinical)CREB1Proto-Oncogene Proteins c-fosSignal TransductionTranscription FactorsDevelopmental BiologyBrain Research
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Estrogen receptor (ER)-mediated transcriptional regulation of the human corticotropin-releasing hormone-binding protein promoter: differential effect…

2004

CRH-binding protein (CRH-BP) regulates activation of the hypothalamic-pituitary-adrenal (HPA) axis by binding and inhibiting CRH. We investigated for the first time transcriptional regulation of the human CRH-BP promoter using transient transfections. Estrogen receptors (ERs) contributed to ligand-independent constitutive activation of the promoter, whereas in the presence of estradiol ERalpha induced and ERbeta repressed promoter activity in a dose-dependent manner. TNFalpha inhibited promoter induction by ERalpha in the absence and presence of estradiol. Three ERE half-sites in the CRH-BP promoter bound ERalpha and ERbeta in an EMSA, and disruption of ERE half-sites by site-directed mutag…

Transcriptional Activationendocrine systemTranscription Geneticmedicine.drug_classResponse elementEstrogen receptorBiologyResponse ElementsEndocrinologymedicineTranscriptional regulationTumor Cells CulturedAnimalsEstrogen Receptor betaHumansPromoter Regions GeneticMolecular BiologyPsychological repressionConserved SequenceEstradiolNeurosecretionTumor Necrosis Factor-alphaEstrogen AntagonistsEstrogen Receptor alphaGeneral MedicineTransfectionMolecular biologyTamoxifenEstrogenPituitary GlandMutationTumor necrosis factor alphaCarrier Proteinshormones hormone substitutes and hormone antagonistsTamoxifenmedicine.drugMolecular endocrinology (Baltimore, Md.)
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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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Heme oxygenase-1 induction modulates microsomal prostaglandin E synthase-1 expression and prostaglandin E2 production in osteoarthritic chondrocytes

2009

Pro-inflammatory cytokines such as interleukin-1beta (IL-1beta) may participate in the pathogenesis of cartilage damage in osteoarthritis (OA) through the production of catabolic enzymes and inflammatory mediators. Induction of heme oxygenase-1 (HO-1) has previously been shown to exert anti-inflammatory effects in different cell types. We have investigated whether HO-1 induction may modify chondrocyte viability and the production of relevant mediators such as oxidative stress and prostaglandin E(2) (PGE(2)) elicited by IL-1beta in OA chondrocytes. Chondrocytes were isolated from OA cartilage and used in primary culture. Cells were stimulated with IL-1beta in the absence or presence of the H…

Transcriptional Activationmedicine.medical_specialtyCell Survivalmedicine.medical_treatmentBiologymedicine.disease_causeProstaglandin E synthaseBiochemistryDinoprostoneChondrocyteChondrocytesMicrosomesInternal medicineOsteoarthritismedicineHumansProstaglandin E2Cells CulturedAggrecanProstaglandin-E SynthasesPharmacologyCOPPMolecular biologyIntramolecular OxidoreductasesHeme oxygenasemedicine.anatomical_structureEndocrinologybiology.proteinHeme Oxygenase-1Oxidative stressProstaglandin Emedicine.drugBiochemical Pharmacology
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Interactions between cholinergic and fibroblast growth factor receptors in brain trophism and plasticity

2014

Acetylcholine, acting on both nicotinic receptors (nAChRs) and muscarinic receptors (mAChRs), plays a role in the regulation of synaptic plasticity, being involved in the regulation of cellular processes and cognitive functions, such as learning, memory and attention. Recently, G protein coupled receptors (GPCRs), including mAChRs, have been reported to transactivate tyrosine-kinase receptors (RTK), such as epidermal growth factor receptor (EGFR), and initiate their intracellular signaling. In this minireview we have first analysed the RTK transactivation mechanisms, involving cholinergic receptors, and thereafter the interplay between AChR and neurotrophic factor systems built up by FGF2 a…

Transcriptional Activationmedicine.medical_specialtyClass C GPCRG protein coupled receptorBiologyCholinergic AgonistsBiochemistrySynaptic plasticityTransactivationNicotinic receptorNeurotrophic factorsInternal medicinemedicineAnimalsHumansReceptors CholinergicProtein Interaction MapsReceptorMolecular BiologyG protein-coupled receptorTransactivationNeuronal PlasticityFibroblast growth factor receptor 1Muscarinic receptorBrainReceptor Protein-Tyrosine KinasesCell BiologyGeneral MedicineReceptors Fibroblast Growth FactorErbB ReceptorsEndocrinologyFGFR1Fibroblast growth factor receptorFGFR1; G protein coupled receptor; Muscarinic receptors; Nicotinic receptors; Receptor-receptor interaction; Synaptic plasticity; Transactivation; Tyrosine-kinase receptorsSignal transductionTyrosine-kinase receptorsNeuroscienceReceptor-receptor interactionSignal Transduction
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Histamine Upregulates Gene Expression of Endothelial Nitric Oxide Synthase in Human Vascular Endothelial Cells

2003

Background— Histamine has a short-term, transient, stimulating effect on endothelial nitric oxide synthase (eNOS) activity; however, long-term effects on eNOS have not been described yet. In addition, the vascular effect of histamine seems to depend critically on eNOS functionality. Therefore, we studied the effects of histamine on eNOS gene expression and function. Methods and Results— In human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA.hy 926 cells, histamine upregulated eNOS mRNA (RNase protection assay) and protein (electron microscopic immunocytochemistry) expression. The upregulation of eNOS could be prevented by mepyramine, a selective antagonist at the H 1 recep…

Transcriptional Activationmedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumHistamine H1 receptorNitric OxideCell LineNitric oxidechemistry.chemical_compoundEnosPhysiology (medical)Internal medicinemedicineHumansRNA MessengerReceptors Histamine H1Enzyme InhibitorsPromoter Regions GeneticProtein Kinase InhibitorsCells CulturedDose-Response Relationship DrugbiologyNitric Oxide Synthase Type IIIbiology.organism_classificationMolecular biologyUp-RegulationNitric oxide synthaseKineticsOxidative StressEndocrinologymedicine.anatomical_structurechemistryEnzyme InductionCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinEndothelium VascularNitric Oxide SynthaseHistamine H3 receptorCalcium-Calmodulin-Dependent Protein Kinase Type 2Reactive Oxygen SpeciesCardiology and Cardiovascular MedicineHistamineHistamineCirculation
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