Search results for "CCAAT-Enhancer-Binding Protein"

showing 4 items of 24 documents

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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Transcriptional activation of the small GTPase gene rhoB by genotoxic stress is regulated via a CCAAT element

2001

The gene encoding the Ras-related GTPase RhoB-specific is immediate-early inducible by genotoxic treatments. Regulation of transcriptional activation of rhoB is still unclear. Here we show that cells lacking either p53 or c-Fos are not different from wild-type cells with respect to the level of rhoB induction upon UV irradiation, indicating that these transcription factors are not crucial for stimulation of rhoB mRNA expression. Extracts from UV-irradiated and non-irradiated cells revealed similar DNA-binding activities to a 0.17 kb rhoB promoter fragment harboring the functional element(s) necessary for stimulation of rhoB by UV light. By means of immunoprecipitation we found that an ATF-2…

Transcriptional ActivationImmunoprecipitationUltraviolet RaysRHOBMolecular Sequence DataCAAT boxOligonucleotidesBiologyResponse ElementsArticlechemistry.chemical_compoundMiceRhoB GTP-Binding ProteinGeneticsAnimalsSmall GTPaseRNA MessengerPromoter Regions GeneticrhoB GTP-Binding ProteinTranscription factorBinding SitesCcaat-enhancer-binding proteinsBase Sequence3T3 CellsDNAMolecular biologyMethyl methanesulfonatechemistryCCAAT-Binding FactorMutationCCAAT-Enhancer-Binding ProteinsProtein BindingTranscription Factors
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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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Sense and Antisense DMPK RNA Foci Accumulate in DM1 Tissues during Development.

2015

International audience; Myotonic dystrophy type 1 (DM1) is caused by an unstable expanded CTG repeat located within the DMPK gene 3'UTR. The nature, severity and age at onset of DM1 symptoms are very variable in patients. Different forms of the disease are described, among which the congenital form (CDM) is the most severe. Molecular mechanisms of DM1 are well characterized for the adult form and involve accumulation of mutant DMPK RNA forming foci in the nucleus. These RNA foci sequester proteins from the MBNL family and deregulate CELF proteins. These proteins are involved in many cellular mechanisms such as alternative splicing, transcriptional, translational and post-translational regul…

musculoskeletal diseasesCCAAT-Enhancer-Binding Protein-deltacongenital hereditary and neonatal diseases and abnormalities[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiologylcsh:MedicineMice Transgenic[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMyotonin-Protein KinaseMice[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsHumansMyotonic DystrophyRNA AntisenseRNA Messengerlcsh:ScienceMuscle SkeletalCell NucleusMyocardiumlcsh:R[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyBrainGene Expression Regulation DevelopmentalRNA-Binding Proteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyEmbryo MammalianAlternative SplicingDisease Models Animal[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAnimals Newborn[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]lcsh:QTrinucleotide Repeat ExpansionSignal TransductionResearch ArticlePloS one
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