Search results for "ALPHA"

showing 10 items of 3228 documents

Role of hepatocyte nuclear factor 3γ in the expression of human CYP2C genes

2004

Hepatocyte nuclear factor 3 gamma (HNF-3 gamma) is an important transcription factor for the maintenance of specific liver functions. However, its relevance in the expression of human cytochrome P450 (CYP) genes has not yet been explored. Several HNF3 putative binding sites can be identified in human CYP2C 5'-flanking regions. Gene reporter experiments with proximal promoters revealed that HNF-3 gamma transactivated CYP2C8, CYP2C9, and CYP2C19 (25-, 4-, and 4-fold, respectively), but it did not transactivate CYP2C18. However, overexpression of HNF-3 gamma in hepatoma cells by means of a recombinant adenovirus induced CYP2C9, CYP2C18, and CYP2C19 mRNA (4.5-, 20-, and 50-fold, respectively) b…

Transcriptional ActivationRecombinant Fusion ProteinsGenetic VectorsBiophysicsBiologyHydroxamic AcidsTransfectionBiochemistryGene Expression Regulation EnzymologicAdenoviridaeCytochrome P-450 Enzyme SystemSp3 transcription factorCell Line TumormedicineHumansRNA MessengerEnzyme InhibitorsLuciferasesPromoter Regions GeneticMolecular BiologyTranscription factorBinding SitesNuclear ProteinsPromoterMolecular biologyDNA-Binding ProteinsHistone Deacetylase InhibitorsHepatocyte nuclear factorsTrichostatin AHepatocyte nuclear factor 4Hepatocyte nuclear factor 4 alphaHepatocytesFOXA2Transcription Initiation SiteHepatocyte Nuclear Factor 3-gammaHeLa CellsTranscription Factorsmedicine.drugArchives of Biochemistry and Biophysics
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Transcriptional Regulation of Human CYP3A4 Basal Expression by CCAAT Enhancer-Binding Protein α and Hepatocyte Nuclear Factor-3γ

2003

Cytochrome P450 3A4 (CYP3A4) is involved in the metabolism of more than 50% of currently used therapeutic drugs, yet the mechanisms that control CYP3A4 basal expression in liver are poorly understood. Several putative binding sites for CCAAT/enhancer-binding protein (C/EBP) and hepatic nuclear factor 3 (HNF-3) were found by computer analysis in CYP3A4 promoter. The use of reporter gene assays, electrophoretic mobility shift assays, and site-directed mutagenesis revealed that one proximal and two distal C/EBP alpha binding sites are essential sites for the trans-activation of CYP3A4 promoter. No trans-activation was found in similar reporter gene experiments with a HNF-3 gamma expression vec…

Transcriptional ActivationTranscription GeneticGenetic VectorsBiologyTransfectiondigestive systemGene Expression Regulation EnzymologicChromatin remodelingAdenoviridaeCytochrome P-450 Enzyme SystemCCAAT-Enhancer-Binding Protein-alphamedicineCytochrome P-450 CYP3AHumansEnzyme InhibitorsBinding sitePromoter Regions GeneticCells CulturedPharmacologyReporter geneExpression vectorCcaat-enhancer-binding proteinsNuclear ProteinsMolecular biologyChromatinDNA-Binding ProteinsHistone Deacetylase InhibitorsHepatocyte nuclear factorsTrichostatin AHepatocytesMolecular MedicineHepatocyte Nuclear Factor 3-gammaTranscription Factorsmedicine.drugMolecular Pharmacology
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Hypoxia-inducible factor 1Α may regulate the commitment of mesenchymal stromal cells toward angio-osteogenesis by mirna-675-5P

2017

Abstract Background aims During bone formation, angiogenesis and osteogenesis are regulated by hypoxia, which is able to induce blood vessel formation, as well as recruit and differentiate human mesenchymal stromal cells (hMSCs). The molecular mechanisms involved in HIF-1α response and hMSC differentiation during bone formation are still unclear. This study aimed to investigate the synergistic role of hypoxia and hypoxia-mimetic microRNA miR-675-5p in angiogenesis response and osteo-chondroblast commitment of hMSCs. Methods By using a suitable in vitro cell model of hMSCs (maintained in hypoxia or normoxia), the role of HIF-1α and miR-675-5p in angiogenesis and osteogenesis coupling was inv…

Transcriptional ActivationVascular Endothelial Growth Factor A0301 basic medicineCancer ResearchAngiogenesisCellular differentiationImmunologyNeovascularization PhysiologicBiology03 medical and health scienceschemistry.chemical_compoundOsteogenesisMiR-675-5pmedicineHumansImmunology and AllergyHypoxiaCells Culturedbeta CateninGenetics (clinical)TransplantationOsteoblastsMesenchymal stromal cellMesenchymal stem cellWnt signaling pathwayCell DifferentiationMesenchymal Stem CellsOsteoblastCell BiologyHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaUp-RegulationCell biologyVascular endothelial growth factorMicroRNAsVascular endothelial growth factor A030104 developmental biologymedicine.anatomical_structureGene Expression RegulationOncologyHypoxia-inducible factorschemistryRegenerative medicineImmunologyOsteoblast commitmentCytotherapy
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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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The yopJ locus is required for Yersinia-mediated inhibition of NF-kappaB activation and cytokine expression: YopJ contains a eukaryotic SH2-like doma…

1998

Upon exposure to bacteria, eukaryotic cells activate signalling pathways that result in the increased expression of several defence-related genes. Here, we report that the yopJ locus of the enteropathogen Yersinia pseudotuberculosis encodes a protein that inhibits the activation of NF-kappaB transcription factors by a mechanism(s), which prevents the phosphorylation and subsequent degradation of the inhibitor protein IkappaB. Consequently, eukaryotic cells infected with YopJ-expressing Yersinia become impaired in NF-kappaB-dependent cytokine expression. In addition, the blockage of inducible cytokine production coincides with yopJ-dependent induction of apoptosis. Interestingly, the YopJ pr…

Transcriptional Activationmedicine.medical_treatmentMolecular Sequence DataApoptosisBiologySH2 domainTransfectionMicrobiologysrc Homology DomainsGenes ReportermedicineYersinia pseudotuberculosisHumansAmino Acid SequenceMolecular BiologyGeneTranscription factorCells CulturedSrc homology domainVirulenceTumor Necrosis Factor-alphaMacrophagesNF-kappa BYersiniosisGene Expression Regulation Bacterialbiology.organism_classificationmedicine.diseaseFlow CytometryMolecular biologyCell biologyCytokineYersinia pseudotuberculosisPhosphorylationCytokinesBacterial Outer Membrane ProteinsHeLa CellsPlasmidsMolecular microbiology
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Ionizing radiation-induced E-selectin gene expression and tumor cell adhesion is inhibited by lovastatin and all-trans retinoic acid

2004

E-selectin mediated tumor cell adhesion plays an important role in metastasis. Here we show that ionizing radiation (IR) induces E-selectin gene and protein expression in human endothelial cells at therapeutically relevant dose level. E-selectin expression is accompanied by an increase in the adhesion of human colon carcinoma cells to primary human umbilical vein endothelial cells (HUVEC). The HMG-CoA reductase inhibitor lovastatin impairs IR-stimulated E-selectin expression as analyzed at the level of the protein, mRNA and promoter. Inactivation of Rho GTPases either by use of Clostridium difficile toxin A or by co-expression of dominant-negative Rho blocked IR-induced E-selectin gene indu…

Transcriptional Activationrho GTP-Binding ProteinsCancer ResearchBlotting WesternIntercellular Adhesion Molecule-1Retinoic acidEnzyme-Linked Immunosorbent AssayTretinoinchemistry.chemical_compoundGenes ReporterTretinoinCell Line TumorNeoplasmsRadiation IonizingE-selectinGene expressionCell AdhesionmedicineHumansLovastatinRNA MessengerPromoter Regions GeneticCell adhesionCells CulturedDose-Response Relationship DrugbiologyReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaCell adhesion moleculeNF-kappa BDose-Response Relationship RadiationGeneral MedicineIntercellular Adhesion Molecule-1Gene Expression Regulation Neoplasticchemistrybiology.proteinCancer researchEndothelium VascularLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsE-Selectinmedicine.drugCarcinogenesis
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Bleomycin induced pulmonary toxicity and its subpleural onset

2016

Idiopathic Pulmonary Fibrosis (PF) is a rare and devastating disease without efficient treatment at this time. Idiopathic FP is characterized by accumulation of myofibroblasts and has a typical sub-pleural onset suggesting a role of the pleura in the disease. Transforming Growth Factor (TGF)-ß1 induces transformation of pleural mesothelial cells (PMC) into active cells exhibiting myofibroblast phenotype. Heat shock proteins can act as regulator of the TGF-ß1 signaling. A role for caspase-1/IL-1ß axis has already been described in animal models of PF.The heat shock protein AlphaB-crystallin has been studied in PF at the PMC level and the importance of caspase-1/IL-1ß axis has been investigat…

Transforming Growth Factor-β1Cellules mésothéliales pleuralesTransition épithélio-mésenchymateuseBléomycineCaspase-1AlphaB-crystallin[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyFibrose pulmonaire idiopatique[SDV.BC] Life Sciences [q-bio]/Cellular Biology
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Hydrodynamic liver gene transfer mechanism involves transient sinusoidal blood stasis and massive hepatocyte endocytic vesicles

2005

The present study contributes to clarify the mechanism underlying the high efficacy of hepatocyte gene transfer mediated by hydrodynamic injection. Gene transfer experiments were performed employing the hAAT gene, and the efficacy and differential identification in mouse plasma of human transgene versus mouse gene was assessed by ELISA and proteomic procedures, respectively. By applying different experimental strategies such as cumulative dose-response efficacy, hemodynamic changes reflected by venous pressures, intravital microscopy, and morphological changes established by transmission electron microscopy, we found that: (a) cumulative multiple doses of transgene by hydrodynamic injection…

TransgeneGenetic VectorsMolecular Sequence DataEnzyme-Linked Immunosorbent AssayVena Cava InferiorBlood stasisGene deliveryBiologyMiceGeneticsmedicineAnimalsHumansMolecular BiologyPortal VeinCytoplasmic VesiclesGenetic transferGene Transfer TechniquesBlood flowMolecular biologyEndocytosisCell biologyMice Inbred C57BLMicroscopy ElectronEndocytic vesiclemedicine.anatomical_structurealpha 1-AntitrypsinHepatocyteHepatocytesMolecular MedicineVenous PressureIntravital microscopyLiver CirculationGene Therapy
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Interleukin-7 matures suppressive CD127(+) forkhead box P3 (FoxP3)(+) T cells into CD127(-) CD25(high) FoxP3(+) regulatory T cells.

2011

We have identified a novel interleukin (IL)-7-responsive T cell population [forkhead box P3 (FoxP3(+) ) CD4(+) CD25(+) CD127(+) ] that is comparably functionally suppressive to conventional FoxP3(+) CD4(+) CD25(+) regulatory T cells (T(regs) ). Although IL-2 is the most critical cytokine for thymic development of FoxP3(+) T(regs) , in the periphery other cytokines can be compensatory. CD25(+) CD127(+) T cells treated with IL-7 phenotypically 'matured' into the known 'classical' FoxP3(+) CD4(+) CD25(high) CD127(-) FoxP3(+) T(regs) . In freshly isolated splenocytes, the highest level of FoxP3 expression was found in CD127(+) CD25(+) T cells when compared with CD127(-) CD25(+) or CD127(+) CD25…

Translational StudiesT cellImmunologyActive Transport Cell Nucleuschemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryInterleukin-7 Receptor alpha SubunitInterleukin 21MiceAntigenAntigens CDT-Lymphocyte SubsetsmedicineImmunology and AllergyCytotoxic T cellAnimalsCTLA-4 AntigenIL-2 receptorInterleukin-7 receptorCells CulturedCell NucleusMice Inbred BALB CInterleukin-7autoimmunityInterleukin-2 Receptor alpha SubunitFOXP3virus diseaseshemic and immune systemsCell DifferentiationForkhead Transcription FactorsT lymphocyteMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationImmunologyLeukocyte Common AntigensFoxP3 TregClinical and experimental immunology
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