Search results for "CCAAT-Enhancer-Binding Protein-beta"

showing 5 items of 5 documents

Hepatogenic differentiation of human mesenchymal stem cells from adipose tissue in comparison with bone marrow mesenchymal stem cells

2006

AIM: To investigate and compare the hepatogenic transdifferentiation of adipose tissue-derived stem cells (ADSC) and bone marrow-derived mesenchymal stem cells (BMSC) in vitro. Transdifferentiation of BMSC into hepatic cells in vivo has been described. Adipose tissue represents an accessible source of ADSC, with similar characteristics to BMSC. METHODS: BMSCs were obtained from patients undergoing total hip arthroplasty and ADSC from human adipose tissue obtained from lipectomy. Cells were grown in medium containing 15% human serum. Cultures were serum deprived for 2 d before cultivating under similar pro-hepatogenic conditions to those of liver development using a 2-step protocol with sequ…

AdultTranscriptional ActivationPathologymedicine.medical_specialtyCellular differentiationAdipose tissueBone Marrow CellsBiologyStem cell markerCytochrome P-450 Enzyme SystemClinical ResearchAlbuminsCell Line TumormedicineCytochrome P-450 CYP3AHumansCells CulturedAgedCCAAT-Enhancer-Binding Protein-betaRegeneration (biology)Mesenchymal stem cellTransdifferentiationGastroenterologyCell DifferentiationCytochrome P-450 CYP2E1Mesenchymal Stem CellsGeneral MedicineMiddle AgedPhenotypeAdipose TissueGene Expression RegulationHepatocyte Nuclear Factor 4HepatocytesHepatic stellate cellCancer researchThy-1 AntigensStem cellWorld Journal of Gastroenterology
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Regulation of IL-12 p40 Promoter Activity in Primary Human Monocytes: Roles of NF-κB, CCAAT/Enhancer-Binding Protein β, and PU.1 and Identification o…

2001

Abstract Appropriate regulation of IL-12 expression is critical for cell-mediated immune responses. In the present study, we have analyzed the regulation of IL-12 p40 promoter activity in primary human monocytes in vivo. Accordingly, we analyzed the p40 promoter by in vivo footprinting in resting and activated primary human blood CD14+ monocytes. Interestingly, footprints at binding sites for trans-activating proteins such as C/EBP, NF-κB, and ETS were only found upon stimulation with LPS and IFN-γ. In contrast, a footprint over a purine-rich sequence at −155, termed GA-12 (GATA sequence in the IL-12 promoter), was observed in resting, but not activated, cells. Further characterization of t…

CD14ImmunologyDNA FootprintingLipopolysaccharide ReceptorsRepressorBiologyDinoprostoneMonocytesCell LineMicechemistry.chemical_compoundProto-Oncogene ProteinsGene expressionAnimalsHumansImmunology and AllergyBinding sitePromoter Regions GeneticPsychological repressionCells CulturedDNA PrimersBase SequenceCcaat-enhancer-binding proteinsCCAAT-Enhancer-Binding Protein-betaBinding proteinNF-kappa BNuclear ProteinsNF-κBInterleukin-12Molecular biologychemistryMutagenesis Site-DirectedTrans-ActivatorsInterleukin-4The Journal of Immunology
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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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Down-regulation of human CYP3A4 by the inflammatory signal interleukin-6: molecular mechanism and transcription factors involved.

2002

The hepatic drug-metabolizing cytochrome P-450 (CYP) enzymes are down-regulated during inflammation. In vitro studies with hepatocytes have shown that the cytokines released during inflammatory responses are largely responsible for this CYP repression. However, the signaling pathways and the cytokine-activated factors involved remain to be properly identified. Our research has focused on the negative regulation of CYP3A4 (the major drug-metabolizing human CYP) by interleukin 6 (IL-6) (the principal regulator of the hepatic acute-phase response). CYP3A4 down-regulation by IL-6 requires activation of the glycoprotein receptor gp130; however, it does not proceed through the JAK/STAT pathway, a…

MAPK/ERK pathwaySTAT3 Transcription FactorMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesDown-RegulationBiologyBiochemistryTransactivationCytochrome P-450 Enzyme SystemAntigens CDGeneticsCCAAT-Enhancer-Binding Protein-alphaCytokine Receptor gp130Tumor Cells CulturedCytochrome P-450 CYP3AHumansRNA MessengerSTAT3Molecular BiologyTranscription factorCells CulturedMembrane GlycoproteinsDose-Response Relationship DrugInterleukin-6Reverse Transcriptase Polymerase Chain ReactionCCAAT-Enhancer-Binding Protein-betaJAK-STAT signaling pathwayProtein-Tyrosine KinasesGlycoprotein 130Molecular biologyDNA-Binding ProteinsGene Expression Regulationbiology.proteinHepatocytesTrans-ActivatorsSignal transductionBiotechnologyAcute-Phase ProteinsSignal TransductionTranscription FactorsFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Glucocorticoid receptor regulates organic cation transporter 1 (OCT1, SLC22A1) expression via HNF4α upregulation in primary human hepatocytes

2013

Abstract Background Organic cation transporter 1 (OCT1, SLC22A1) is a membrane transporter that is important for therapeutic effect of the antidiabetic drug metformin. Its liver-specific expression in hepatocytes is strongly controlled by hepatocyte nuclear factor-4α (HNF4α). HNF4α expression and transcriptional activity have been demonstrated to be augmented by glucocorticoid receptor (GR) in human hepatocytes and rodent livers. Methods It was examined whether GR activation indirectly induces OCT1 gene expression via HNF4α up-regulation in primary human hepatocytes.We also examined which other transcription factors are involved in OCT1 gene expression and whether they are regulated by dexa…

Time FactorsPrimary Cell CultureTransfectionDexamethasoneReceptors GlucocorticoidGlucocorticoid receptorTransduction GeneticEnhancer bindingCoactivatorGene expressionHumansRNA MessengerGlucocorticoidsTranscription factorPharmacologyRegulation of gene expressionChemistryCCAAT-Enhancer-Binding Protein-betaOrganic Cation Transporter 1Hep G2 CellsGeneral MedicineTransfectionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMolecular biologyUp-RegulationHepatocyte Nuclear Factor 4Cell cultureHepatocytesTranscription FactorsPharmacological Reports
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