Search results for "transactivation"

showing 10 items of 54 documents

Patchwork Pattern of Transcriptional Reactivation in the Lungs Indicates Sequential Checkpoints in the Transition from Murine Cytomegalovirus Latency…

1999

The lungs are a relevant organ site of primary and recurrent human cytomegalovirus (hCMV) disease (for overviews, see references 21, 22, 31, 34, 39, and 44). Murine CMV (mCMV) can serve us as a model for studying CMV pneumonia in acute infection (6, 27, 33, 37) as well as for studying viral latency, reactivation, and recurrence in the lungs (2, 17, 18, 42, 43). We have shown recently that transcription from the major immediate-early (MIE) transcription unit ie1-ie3 (hereafter referred to as ie1/3), which is driven by a strong MIE promoter-enhancer (MIEPE) (3), occurs during pulmonary latency of mCMV but fails to initiate the productive cycle (17). Notably, the paralogous MIEPE of hCMV can f…

Gene Expression Regulation ViralTranscriptional ActivationHuman cytomegalovirusvirusesImmunologyCytomegalovirusReplicationBiologyMicrobiologyMiceTransactivationTranscription (biology)VirologyGene expressionVirus latencymedicineAnimalsEnhancerGenes Immediate-EarlyLungTranscription factorMice Inbred BALB CEffectormedicine.diseaseVirologyVirus LatencyInsect ScienceCytomegalovirus InfectionsFemaleVirus ActivationTranscription FactorsJournal of Virology
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ΔNp73β is oncogenic in hepatocellular carcinoma by blocking apoptosis signaling via death receptors and mitochondria

2010

p73 belongs to the p53 family of transcription factors known to regulate cell cycle and apoptosis. The Trp73 gene has two promoters that drive the expression of two major p73 isoform subfamilies: TA and ΔN. In general, TAp73 isoforms show proapoptotic activities, whereas members of the N-terminally truncated (ΔN) p73 subfamily that lack the transactivation domain show antiapoptotic functions. We found that upregulation of ΔNp73 in hepatocellular carcinoma (HCC) correlated with reduced survival. Here, we investigated the molecular mechanisms accounting for the oncogenic role of ΔNp73 in HCC.ΔNp73β can directly interfere with the transcriptional activation function of the TA (containing the t…

Gene isoformCarcinoma HepatocellularMolecular Sequence DataApoptosisBiologyModels BiologicalTransactivationDownregulation and upregulationCell Line TumorHumansProtein IsoformsMolecular BiologyTranscription factorGenes DominantOligonucleotide Array Sequence Analysisbcl-2-Associated X ProteinRegulation of gene expressionBase SequenceSettore BIO/11Gene Expression ProfilingTumor Suppressor ProteinsLiver NeoplasmsNuclear ProteinsTumor Protein p73PromoterReceptors Death DomainCell BiologyCell cyclePrognosisMitochondriaCell biologyDNA-Binding ProteinsEnzyme ActivationGene Expression Regulation NeoplasticDrug Resistance NeoplasmCaspasesCancer researchTumor Suppressor Protein p53Signal transductionPrecancerous ConditionsSignal TransductionDevelopmental BiologyCell Cycle
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HIF-1α induces MXI1 by alternate promoter usage in human neuroblastoma cells

2009

Adaptation to low oxygen conditions is essential for maintaining homeostasis and viability in oxygen-consuming multi-cellular tissues, including solid tumors. Central in these processes are the hypoxia-inducible transcription factors, HIF-1 and HIF-2, controlling genes involved in e.g. glucose metabolism and neovascularization. Tumor hypoxia and HIF expression have also been associated with a dedifferentiated phenotype and increased aggressiveness. In this report we show that the MAX interactor-1 (MXI1) gene is directly regulated by HIF proteins in neuroblastoma and breast cancer cells. HIF-binding and transactivation were detected within MXI1 gene regulatory sequences in the vicinity of th…

Gene isoformGenes mycBreast NeoplasmsBiologyTransfectionNeuroblastomaTransactivationCell Line TumorNeuroblastomaBasic Helix-Loop-Helix Transcription FactorsmedicineHumansGenes Tumor SuppressorRNA Small InterferingPromoter Regions GeneticGeneTranscription factorOligonucleotide Array Sequence AnalysisBase SequenceTumor hypoxiaTumor Suppressor ProteinsCell BiologyHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseCell HypoxiaUp-RegulationGene Expression Regulation NeoplasticHIF1ARegulatory sequenceCancer researchFemaleExperimental Cell Research
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p63 Isoforms Regulate Metabolism of Cancer Stem Cells

2014

p63 is an important regulator of epithelial development expressed in different variants containing (TA) or lacking (ΔN) the N-terminal transactivation domain. The different isoforms regulate stem-cell renewal and differentiation as well as cell senescence. Several studies indicate that p63 isoforms also play a role in cancer development; however, very little is known about the role played by p63 in regulating the cancer stem phenotype. Here we investigate the cellular signals regulated by TAp63 and ΔNp63 in a model of epithelial cancer stem cells. To this end, we used colon cancer stem cells, overexpressing either TAp63 or ΔNp63 isoforms, to carry out a proteomic study by chemical-labeling …

Gene isoformProteomicsProteomeRegulatorBiologyProteomicsBiochemistryTransactivationCancer stem cellmedicineHumansMetabolomicsProtein IsoformsProtein Interaction MapsSettore BIO/10 - BIOCHIMICAp63 colon cancer stem cells proteomics stable isotope dimethyl labeling glucose metabolismSettore BIO/12Tumor Suppressor ProteinsCancerGeneral Chemistrymedicine.diseasePhenotypePeptide FragmentsCell biologyIsotope LabelingNeoplastic Stem CellsStem cellSignal TransductionTranscription Factors
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Selective Activation of Trophoblast-specific PLAC1 in Breast Cancer by CCAAT/Enhancer-binding Protein β (C/EBPβ) Isoform 2

2009

The trophoblast-specific gene PLAC1 (placenta-specific 1) is ectopically expressed in a wide range of human malignancies, most frequently in breast cancer, and is essentially involved in cancer cell proliferation, migration, and invasion. Here we show that basal activity of the PLAC1 promoter is selectively controlled by ubiquitous transcription factor SP1 and isoform 2 of CCAAT/enhancer-binding protein beta that we found to be selectively expressed in placental tissue and cancer cells. Binding of both factors to their respective elements within the PLAC1 promoter was essential to attain full promoter activity. Estrogen receptor alpha (ERalpha) signaling further augmented transcription and …

Gene isoformSp1 Transcription FactorMolecular Sequence DataEstrogen receptorBreast NeoplasmsPregnancy ProteinsBiologyBiochemistryTransactivationMolecular Basis of Cell and Developmental BiologyTranscription (biology)Cell Line TumorGene expressionHumansProtein IsoformsPromoter Regions GeneticMolecular BiologyCell ProliferationSp1 transcription factorBase SequenceCcaat-enhancer-binding proteinsCCAAT-Enhancer-Binding Protein-betaEstrogen Receptor alphaEstrogensCell BiologyMolecular biologyTrophoblastsGene Expression Regulation NeoplasticChromatin immunoprecipitationJournal of Biological Chemistry
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Nfatc1/Αa and Blimp-1 Support the Follicular and Effector Phenotype of Tregs

2021

CD4 + CXCR5 + Foxp3 + T follicular regulatory (T FR ) cells control the germinal center responses. Like follicular helper T-cells, they express high levels of N uclear F actor of A ctivated T -cells c1 , predominantly its short isoform NFATc1/αA. Ablation of NFATc1 in Tregs prevents upregulation of CXCR5 and migration of T FR cells into B-cell follicles. By contrast, constitutive active NFATc1/αA defines the surface density of CXCR5, whose level determines how deep a T FR migrates into the GC and how effectively it controls antibody production. NFATc1/αA is necessary to overcome T FR -expressed B l ymphocyte- i nduced m aturation p rotein (Blimp-1), which can directly repress Cxcr5. Blimp-1…

Gene isoformTransactivationintegumentary systemDownregulation and upregulationChemistryEffectorGerminal centerFOXP3PhenotypeCXCR5Cell biologySSRN Electronic Journal
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The human liver fatty acid binding protein (FABP1) gene is activated by FOXA1 and PPARα; and repressed by C/EBPα: Implications in FABP1 down-regulati…

2013

Liver fatty acid binding protein (FABP1) prevents lipotoxicity of free fatty acids and regulates fatty acid trafficking and partition. Our objective is to investigate the transcription factors controlling the human FABP1 gene and their regulation in nonalcoholic fatty liver disease (NAFLD). Adenovirus-mediated expression of multiple transcription factors in HepG2 cells and cultured human hepatocytes demonstrated that FOXA1 and PPARα are among the most effective activators of human FABP1, whereas C/EBPα is a major dominant repressor. Moreover, FOXA1 and PPARα induced re-distribution of FABP1 protein and increased cytoplasmic expression. Reporter assays demonstrated that the major basal activ…

Hepatocyte Nuclear Factor 3-alphaMaleRepressorBiologyFatty Acid-Binding ProteinsFatty acid-binding proteinMiceTransactivationNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseCCAAT-Enhancer-Binding Protein-alphamedicineAnimalsHumansPPAR alphaadipocyte protein 2Molecular BiologyTranscription factorCells Culturedchemistry.chemical_classificationFatty acidHep G2 CellsCell Biologymedicine.diseaseMolecular biologyFatty LiverMice Inbred C57BLLipotoxicitychemistrybiology.proteinProtein BindingBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
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Focal Transcriptional Activity of Murine Cytomegalovirus during Latency in the Lungs

1999

ABSTRACT Interstitial pneumonia is a frequent and critical manifestation of human cytomegalovirus (CMV) disease in immunocompromised patients, in particular in recipients of bone marrow transplantation. Previous work in the murine CMV infection model has identified the lungs as a major organ site of CMV latency and recurrence. It was open to question whether the viral genome is transcriptionally silent or active during latency. Transcription could be latency associated and thus be part of the latency phenotype. Alternatively, transcriptional activity could reflect episodes of reactivation. We demonstrate here that transcription of the immediate-early (IE) transcription unit ie1-ie3 selectiv…

Human cytomegalovirusMaleMuromegalovirusTranscription GeneticRNA SplicingImmunologyReplicationBiologyMicrobiologyTransactivationExonMiceMuromegalovirusTranscription (biology)Bone MarrowRecurrenceVirologyVirus latencyGene expressionmedicineAnimalsGeneGenes Immediate-EarlyLungExonsmedicine.diseasebiology.organism_classificationVirologyVirus LatencyInsect ScienceImmunologyDNA ViralFemale
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Hyperthermia Enhances CD95-Ligand Gene Expression in T Lymphocytes

2004

Abstract Hyperthermia represents an interesting therapeutic strategy for the treatment of tumors. Moreover, it is able to regulate several aspects of the immune response. Fas (APO-1/CD95) and its ligand (FasL) are cell surface proteins whose interaction activates apoptosis of Fas-expressing targets. In T cells, the Fas-Fas-L system regulates activation-induced cell death, is implicated in diseases in which lymphocyte homeostasis is compromised, and plays an important role during cytotoxic and regulatory actions mediated by these cells. In this study we describe the effect of hyperthermia on activation of the fas-L gene in T lymphocytes. We show that hyperthermic treatment enhances Fas-L-med…

HyperthermiaFas Ligand ProteinFeverT-LymphocytesT cellBlotting WesternImmunologyBiologyLymphocyte ActivationTransfectionFas ligandJurkat CellsTransactivationImmune systemHeat Shock Transcription FactorsLymphocyte homeostasismedicineAnimalsHumansImmunology and AllergyCytotoxic T cellRNA MessengerPromoter Regions GeneticTranscription factorProtein Kinase CMembrane GlycoproteinsNF-kappa BBlotting NorthernCytotoxicity Tests Immunologicmedicine.diseaseMolecular biologyCell biologyDNA-Binding ProteinsTranscription Factor AP-1medicine.anatomical_structureGene Expression RegulationMutationTranscription FactorsThe Journal of Immunology
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Melittin Modulates Keratinocyte Function through P2 Receptor-dependent ADAM Activation

2012

Melittin, the major component of the bee venom, is an amphipathic, cationic peptide with a wide spectrum of biological properties that is being considered as an anti-inflammatory and anti-cancer agent. It modulates multiple cellular functions but the underlying mechanisms are not clearly understood. Here, we report that melittin activates disintegrin-like metalloproteases (ADAMs) and that downstream events likely contribute to the biological effects evoked by the peptide. Melittin stimulated the proteolysis of ADAM10 and ADAM17 substrates in human neutrophil granulocytes, endothelial cells and murine fibroblasts. In human HaCaT keratinocytes, melittin induced shedding of the adhesion molecu…

KeratinocytesCell SurvivalBlotting WesternADAM17 ProteinP2 receptorBiologyModels Biologicalcomplex mixturesBiochemistryMelittinCell LineADAM10 ProteinMicechemistry.chemical_compoundTransactivationAdenosine TriphosphateAnimalsHumansPhosphorylationExtracellular Signal-Regulated MAP KinasesReceptorMolecular BiologyCells CulturedMice KnockoutDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionPurinergic receptorHEK 293 cellstechnology industry and agricultureMembrane ProteinsCell BiologyFibroblastsCadherinsEmbryo MammalianMelittenCell biologyErbB ReceptorsADAM ProteinsHaCaTHEK293 CellschemistryPhosphorylationlipids (amino acids peptides and proteins)Receptors Purinergic P2X7Amyloid Precursor Protein SecretasesJournal of Biological Chemistry
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