Search results for "DOWN-REGULATION"

showing 10 items of 310 documents

Down-regulation of nuclear binding activities of OXBOX-REBOX transcription factors during cellular senescence.

1996

Functional capacity of mitochondria declines during aging and this impairment may have a major role in aging process. Several observations indicate that transcriptional efficiency is reduced during aging. Our purpose was to find out whether aging and cellular senescence affect the nuclear binding activities of transcription factors which bind to OXBOX-REBOX sequence present in promoter regions of numerous nuclear genes encoding mitochondrial proteins. These factors regulate and coordinate the expression of mitochondrial proteins. We observed a strong down-regulation in the nuclear binding activities of OXBOX-REBOX factors in replicatively senesced human WI-38 and IMR-90 fibroblasts. On the …

Cell cycle checkpointNuclear genePhotoagingMolecular Sequence DataBiophysicsDown-RegulationPlasma protein bindingBiologyMitochondrionBiochemistryDownregulation and upregulationmedicineAnimalsHumansRats WistarMolecular BiologyTranscription factorCellular SenescenceCell Line TransformedBase SequenceNuclear ProteinsCell BiologyDNAmedicine.diseaseCell biologyRatsCell cultureProtein BindingTranscription FactorsBiochemical and biophysical research communications
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MicroRNAs: Promising New Antiangiogenic Targets in Cancer

2014

[EN] MicroRNAs are one class of small, endogenous, non-coding RNAs that are approximately 22 nucleotides in length; they are very numerous, have been phylogenetically conserved, and involved in biological processes such as development, differentiation, cell proliferation, and apoptosis. MicroRNAs contribute to modulating the expression levels of specific proteins based on sequence complementarity with their target mRNA molecules and so they play a key role in both health and disease. Angiogenesis is the process of new blood vessel formation from preexisting ones, which is particularly relevant to cancer and its progression. Over the last few years, microRNAs have emerged as critical regulat…

Cell typeDOWN-REGULATIONArticle SubjectAngiogenesisHUMAN BREAST-CANCERMIR-200 FAMILYlcsh:MedicineAngiogenesis InhibitorsReview ArticleBiologyBioinformaticsGeneral Biochemistry Genetics and Molecular BiologyNUCLEAR EXPORTTUMOR ANGIOGENESISNeovascularizationMicroprocessor complexSMALL RNASDownregulation and upregulationNeoplasmsmicroRNAGene expressionmedicineAnimalsHumansMolecular Targeted TherapyPrecision MedicineIN-VIVOGENE-EXPRESSIONGeneral Immunology and MicrobiologyNeovascularization PathologicCell growthlcsh:RMICROBIOLOGIAGeneral MedicineMICROPROCESSOR COMPLEXMicroRNAsENDOTHELIAL GROWTH-FACTORCancer researchmedicine.symptom
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Caveolin and GLT-1 gene expression is reciprocally regulated in primary astrocytes: Association of GLT-1 with non-caveolar lipid rafts

2004

Caveolae represent membrane microdomains acting as integrators of cellular signaling and functional processes. Caveolins are involved in the biogenesis of caveolae and regulate the activity of caveolae-associated proteins. Although caveolin proteins are found in the CNS, the regulation of caveolins in neural cells is poorly described. In the present study, we investigated different modes and mechanisms of caveolin gene regulation in primary rat astrocytes. We demonstrated that activation of cAMP-dependent signaling pathways led to a marked reduction in protein levels of caveolin-1/-2 in cortical astrocytes. Application of transforming growth factor-alpha (TGF-alpha) also resulted in a decre…

Central Nervous SystemCaveolin 2Caveolin 1Down-RegulationGlutamic AcidBiologyCaveolinsHistone DeacetylasesChromatin remodelingRats Sprague-DawleyPhosphatidylinositol 3-KinasesCellular and Molecular NeuroscienceAstrocyte differentiationMembrane MicrodomainsCaveolaeCaveolinCyclic AMPAnimalsRNA MessengerLipid raftCerebral CortexRegulation of gene expressionTransforming Growth Factor alphaRatsCell biologyCaveolin 2Animals NewbornExcitatory Amino Acid Transporter 2Gene Expression RegulationNeurologyAstrocytesCaveolin 1Signal TransductionGlia
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A critical role for Cyclin E in cell fate determination in the central nervous system of Drosophila melanogaster

2004

We have examined the process by which cell diversity is generated in neuroblast (NB) lineages in the central nervous system of Drosophila melanogaster. Thoracic NB6-4 (NB6-4t) generates both neurons and glial cells, whereas NB6-4a generates only glial cells in abdominal segments. This is attributed to an asymmetric first division of NB6-4t, localizing prospero (pros) and glial cell missing (gcm) only to the glial precursor cell, and a symmetric division of NB6-4a, where both daughter cells express pros and gcm. Here we show that the NB6-4t lineage represents the ground state, which does not require the input of any homeotic gene, whereas the NB6-4a lineage is specified by the homeotic genes…

Central Nervous SystemCyclin ELineage (genetic)Cell divisionDown-RegulationNerve Tissue ProteinsCell fate determinationNeuroblastCyclin EAnimalsDrosophila ProteinsCell LineageHomeodomain ProteinsNeuronsbiologyStem CellsNeuropeptidesGenes HomeoboxGene Expression Regulation DevelopmentalNuclear ProteinsCell DifferentiationCell BiologyCell cyclebiology.organism_classificationGanglia InvertebrateCell biologyDNA-Binding ProteinsDrosophila melanogasterTrans-ActivatorsDrosophila melanogasterHomeotic geneNeurogliaTranscription FactorsNature Cell Biology
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Comm Sorts Robo to Control Axon Guidance at the Drosophila Midline

2002

AbstractAxon growth across the Drosophila midline requires Comm to downregulate Robo, the receptor for the midline repellent Slit. We show here that comm is required in neurons, not in midline cells as previously thought, and that it is expressed specifically and transiently in commissural neurons. Comm acts as a sorting receptor for Robo, diverting it from the synthetic to the late endocytic pathway. A conserved cytoplasmic LPSY motif is required for endosomal sorting of Comm in vitro and for Comm to downregulate Robo and promote midline crossing in vivo. Axon traffic at the CNS midline is thus controlled by the intracellular trafficking of the Robo guidance receptor, which in turn depends…

Central Nervous SystemEmbryo NonmammalianEndosomeGrowth ConesMolecular Sequence DataEndocytic cycleDown-RegulationNerve Tissue ProteinsReceptors Cell SurfaceCell CommunicationEndosomesBiologyModels BiologicalFunctional LateralityGeneral Biochemistry Genetics and Molecular BiologySequence Homology Nucleic AcidEctodermmedicineAnimalsDrosophila ProteinsReceptors ImmunologicAxonTransport VesiclesReceptorSequence Homology Amino AcidBiochemistry Genetics and Molecular Biology(all)Stem CellsCell MembraneGraft SurvivalGene Expression Regulation DevelopmentalMembrane ProteinsCell DifferentiationAnatomyCommissureSlitProtein Structure TertiaryCell biologyProtein TransportDrosophila melanogastermedicine.anatomical_structureCOS CellsRoundaboutAxon guidanceStem Cell TransplantationCell
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Influenza A virus infection inhibits the efficient recruitment of Th2 cells into the airways and the development of airway eosinophilia.

2003

Abstract Most infections with respiratory viruses induce Th1 responses characterized by the generation of Th1 and CD8+ T cells secreting IFN-γ, which in turn have been shown to inhibit the development of Th2 cells. Therefore, it could be expected that respiratory viral infections mediate protection against asthma. However, the opposite seems to be true, because viral infections are often associated with the exacerbation of asthma. For this reason, we investigated what effect an influenza A (flu) virus infection has on the development of asthma. We found that flu infection 1, 3, 6, or 9 wk before allergen airway challenge resulted in a strong suppression of allergen-induced airway eosinophil…

ChemokineEpitopes T-LymphocyteImmunoglobulin Emedicine.disease_causeMiceCell MovementInfluenza A virusImmunology and AllergyEosinophiliaChemokine CCL5LungCells CulturedChemokine CCL2Mice KnockoutMice Inbred BALB Cbiologymedicine.diagnostic_testrespiratory systemUp-Regulationmedicine.anatomical_structureInfluenza A virusChemokines CCGoblet CellsNippostrongylusmedicine.symptomBronchial HyperreactivityChemokine CCL11OvalbuminImmunologyDown-RegulationMice TransgenicCCL5VirusInterferon-gammaTh2 CellsOrthomyxoviridae InfectionsLymphopeniamedicineAnimalsLymphocyte CountPulmonary EosinophiliaStrongylida InfectionsGoblet cellMetaplasiaAllergensPeptide Fragmentsrespiratory tract diseasesMice Inbred C57BLBronchoalveolar lavageImmunologyCell Migration Inhibitionbiology.proteinInterleukin-5Journal of immunology (Baltimore, Md. : 1950)
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Down-regulation of early sea urchin histone H2A gene relies on cis regulative sequences located in the 5' and 3' regions and including the enhancer b…

2004

The tandem repeated sea urchin alpha-histone genes are developmentally regulated by gene-specific promoter elements. Coordinate transcription of the five genes begins after meiotic maturation of the oocyte, continues through cleavage, and reaches its maximum at morula stage, after which these genes are shut off and maintained in a silenced state for the life cycle of the animal. Although cis regulative sequences affecting the timing and the level of expression of these genes have been characterized, much less is known about the mechanism of their repression. Here we report the results of a functional analysis that allowed the identification of the sequence elements needed for the silencing …

Chloramphenicol O-Acetyltransferaseanimal structuresEmbryo NonmammalianMicroinjectionsgenomic insulatorDown-RegulationSettore BIO/11 - Biologia MolecolareBiologyRegulatory Sequences Nucleic AcidDNA-binding proteinHistonesStructural BiologyTranscription (biology)Gene expressionHistone H2Atranscriptional repressionGene silencingAnimalsGene SilencingTransgenesEnhancerPromoter Regions GeneticMolecular BiologyGenePsychological repressionhistone geneRepetitive Sequences Nucleic AcidSequence DeletionGeneticsenhancer blockerGastrulaEnhancer Elements GeneticSea Urchinsembryonic structuresProtein BindingJournal of molecular biology
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Down-regulation of transcription factors AP-1, Sp-1, and NF-kappa B precedes myocyte differentiation.

1996

Terminal differentiation of myocytes involves withdrawal from the cell cycle, induction of myogenin expression, and finally formation of myotubes. To study the factors that regulate the initial phase of muscle differentiation, we analyzed the binding activities of transcription factors AP-1, Sp-1, and NF-kappa B in L6, C2C12, and rhabdomyosarcoma BA-Han-1C cells. Temporal changes in transcription factor binding activities were compared to the activation of myogenin promoter-driven CAT reporter gene and the expression level of myogenin, a master gene of myogenic differentiation. We observed a prominent decrease in the nuclear binding activities of AP-1, Sp-1, and NF-kappa B already 12 to 24 …

Cholera ToxinSp1 Transcription FactorCellular differentiationBiophysicsDown-RegulationBiologyMuscle DevelopmentBiochemistryRetinoblastoma ProteinCell FusionMiceOkadaic AcidTumor Cells CulturedMyocyteAnimalsMuscle SkeletalMolecular BiologyTranscription factorMyogeninCell fusionMyogenesisNF-kappa BCell DifferentiationCell BiologyCell cyclemusculoskeletal systemMolecular biologyRatsUp-RegulationTranscription Factor AP-1MyogeninC2C12Protein BindingBiochemical and biophysical research communications
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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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Endoplasmic reticulum‐resident chaperones modulate the inflammatory and angiogenic responses of endothelial cells

2015

SummaryBackground Wound healing depends on a well-balanced regulation of inflammation and angiogenesis. In chronic wounds the healing process is disturbed and inflammation persists. Regulation of wound closure is controlled by transmembrane and extracellular proteins, the folding and maturation of which occur in the endoplasmic reticulum (ER) by ER-resident chaperone machinery. Objectives To study the role of the ER-resident chaperones BiP/Grp78, its cochaperone Mdg1/ERdJ4, and Grp94 in chronic, nonhealing wounds. Methods Immunohistochemical staining of these chaperones in individual human biopsies and investigation of the possible role of BiP and Mdg1 in endothelial cells, focusing on thei…

Chronic woundChemokineAngiogenesisDown-RegulationNeovascularization PhysiologicInflammationDermatologyEndoplasmic ReticulumProinflammatory cytokinemedicineHumansEndoplasmic Reticulum Chaperone BiPCells CulturedHeat-Shock ProteinsInflammationWound HealingMembrane GlycoproteinsbiologyTumor Necrosis Factor-alphaEndoplasmic reticulumEndothelial CellsMembrane ProteinsHSP40 Heat-Shock ProteinsCell biologyChaperone (protein)Chronic Diseasebiology.proteinmedicine.symptomWound healingMolecular ChaperonesBritish Journal of Dermatology
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