Search results for "nuclear factor"

showing 10 items of 84 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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Receptor Activator of NF-kB (RANK) Expression in Primary Tumors Associates with Bone Metastasis Occurrence in Breast Cancer Patients

2011

Background\ud Receptor activator of NFkB (RANK), its ligand (RANKL) and the decoy receptor of RANKL (osteoprotegerin, OPG) play a pivotal role in bone remodeling by regulating osteoclasts formation and activity. RANKL stimulates migration of RANK-expressing tumor cells in vitro, conversely inhibited by OPG.\ud \ud Materials and Methods\ud We examined mRNA expression levels of RANKL/RANK/OPG in a publicly available microarray dataset of 295 primary breast cancer patients. We next analyzed RANK expression by immunohistochemistry in an independent series of 93 primary breast cancer specimens and investigated a possible association with clinicopathological parameters, bone recurrence and surviv…

Anatomy and PhysiologyMicroarraysSettore MED/06 - Oncologia MedicaCancer TreatmentLigandsMetastasisBone remodelingMetastasisBasic Cancer ResearchBreast TumorsBone and Soft Tissue SarcomasNeoplasm MetastasisMusculoskeletal SystemOligonucleotide Array Sequence AnalysisMultidisciplinaryPredictive markerReceptor Activator of Nuclear Factor-kappa BQRBone metastasisMiddle AgedImmunohistochemistryGene Expression Regulation NeoplasticOncologyRANKLMedicineFemaleResearch Articlemusculoskeletal diseasesmedicine.medical_specialtyHistologyScienceBone NeoplasmsBreast NeoplasmsBiologyBreast cancerAntibody TherapySDG 3 - Good Health and Well-beingOsteoprotegerinInternal medicinemedicineHumansRNA MessengerBoneBiologyAgedBreast cancer bone metastasis RANK-RANKLRANK LigandOsteoprotegerinComputational BiologyCancers and NeoplasmsRANK Ligandmedicine.diseaseEndocrinologyCancer researchbiology.protein
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Convergence of Wnt signaling on the HNF4alpha-driven transcription in controlling liver zonation.

2009

Background & Aims: In each hepatocyte, the specific repertoire of gene expression is influenced by its exact location along the portocentrovenular axis of the hepatic lobule and provides a reason for the liver functions compartmentalization defined "metabolic zonation." So far, few molecular players controlling genetic programs of periportal (PP) and perivenular (PV) hepatocytes have been identified; the elucidation of zonation mechanisms remains a challenge for experimental hepatology. Recently, a key role in induction and maintenance of the hepatocyte heterogeneity has been ascribed to Wnt/β-catenin pathway. We sought to clarify how this wide-ranging stimulus integrates with hepatocyte s…

Beta-cateninWnt ProteinCellular differentiationBlotting WesternLiver Stem CellFluorescent Antibody TechniqueMice TransgenicBiologyTransfectionSensitivity and SpecificityAnimals; Blotting Western; Cell Differentiation; Cell Proliferation; Cells Cultured; Fluorescent Antibody Technique; Hepatocyte Nuclear Factor 4; Hepatocytes; Humans; Immunoprecipitation; Mice; Mice Knockout; Mice Transgenic; Reverse Transcriptase Polymerase Chain Reaction; Sensitivity and Specificity; Signal Transduction; Transfection; Wnt Proteins; beta Catenin; GastroenterologyMiceliver zonation; wnt signalling; beta catenin; hnf4Gene expressionmedicineAnimalsHumansImmunoprecipitationHepatocyteCells Culturedbeta CateninCell ProliferationMice KnockoutHepatologyAnimalReverse Transcriptase Polymerase Chain ReactionGastroenterologyWnt signaling pathwayCell DifferentiationMolecular biologyWnt Proteinsmedicine.anatomical_structureHepatocyte nuclear factor 4Hepatocyte Nuclear Factor 4Hepatocytebiology.proteinHepatocytesChromatin immunoprecipitationHumanSignal TransductionGastroenterology
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miR-29b negatively regulates human osteoclastic cell differentiation and function: Implications for the treatment of multiple myeloma-related bone di…

2013

Skeletal homeostasis relies upon a fine tuning of osteoclast (OCLs)-mediated bone resorption and osteoblast (OBLs)-dependent bone formation. This balance is unsettled by multiple myeloma (MM) cells, which impair OBL function and stimulate OCLs to generate lytic lesions. Emerging experimental evidence is disclosing a key regulatory role of microRNAs (miRNAs) in the regulation of bone homeostasis suggesting the miRNA network as potential novel target for the treatment of MM-related bone disease. Here, we report that miR-29b expression decreases progressively during human OCL differentiation in vitro. We found that lentiviral transduction of miR-29b into OCLs, even in the presence of MM cells,…

Bone diseasePhysiologyCellular differentiationCathepsin KClinical BiochemistryGene ExpressionOsteoclastsOsteolysisMMP9Cathepsin KCells CulturedTartrate-resistant acid phosphataseTumorCulturedReceptor Activator of Nuclear Factor-kappa BGenes fosCell DifferentiationOsteoblastCell biologyIsoenzymesmultiple myelomamedicine.anatomical_structureMatrix Metalloproteinase 9osteoclastMatrix Metalloproteinase 2medicine.medical_specialtyfosCellsAcid PhosphataseBiologyCollagen Type IBone resorptionCell LineOsteoclastCell Line TumorInternal medicinemedicineHumansBone ResorptionOsteoblastsmicroRNA.NFATC Transcription FactorsTartrate-Resistant Acid PhosphatasemiR-29bCell Biologymedicine.diseaseActinsMicroRNAsEndocrinologyGenesAcid Phosphatase; Actins; Bone Resorption; Cathepsin K; Cell Differentiation; Cell Line Tumor; Cells Cultured; Collagen Type I; Gene Expression; Genes fos; Humans; Isoenzymes; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; MicroRNAs; Multiple Myeloma; NFATC Transcription Factors; Osteoblasts; Osteoclasts; Osteolysis; Receptor Activator of Nuclear Factor-kappa BJournal of Cellular Physiology
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Epigenetic changes and nuclear factor-κB activation, but not microRNA-224, downregulate Raf-1 kinase inhibitor protein in triple-negative breast canc…

2015

Raf-1 kinase inhibitor protein (RKIP) is a tumor suppressor and metastasis inhibitor, which enhances drug-induced apoptosis of cancer cells. Downregulation of RKIP may be significant in the biology of highly aggressive and drug-resistant tumors, for example triple-negative breast cancers (TNBCs). Potential causes for the low levels of RKIP expressed by SUM 159 TNBC cells were investigated in the present study. Bisulphite modification, methylation specific-polymerase chain reaction (PCR) and a TransAM NF-κB assay were performed and the results suggested that various mechanisms, including methylation of the gene promoter, histone deacetylation and nuclear factor-κB (NF-κB) activation, but not…

Cancer Researchmedicine.drug_classCell growthtriple-negative breast cancer Raf-1 kinase inhibitor protein epigenetic changes microRNA-224 nuclear factor-κBHistone deacetylase inhibitorArticlesCell cycleBiologyMolecular biologyDemethylating agentchemistry.chemical_compoundTrichostatin AOncologychemistryCancer cellmedicineCancer researchGrowth inhibitionTranscription factormedicine.drug
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Re-expression of C/EBP alpha induces CYP2B6, CYP2C9 and CYP2D6 genes in HepG2 cells.

1998

Cytochrome P450 (CYP) activity is very low or even absent in human hepatomas, a phenomenon that is accompanied by low levels of some liver transcription factors, notably C/EBP alpha. To investigate a possible link between this transcription factor and hepatic CYP expression, we have stably transfected HepG2 cells with a C/EBP alpha vector containing a Zn-inducible metallothionein promoter. Expression of functional C/EBP alpha up to liver levels concomitantly increased the mRNAs of several members of the CYP2 family (2B6, 2C9 and 2D6), suggesting that this transcription factor may play a relevant role in controlling the hepatic expression of CYP enzymes.

Carcinoma HepatocellularCYP2B6BiophysicsHepG2 cellTransfectionBiochemistryGene Expression Regulation EnzymologicCytochrome P-450 Enzyme SystemStructural BiologyTumor Cells CulturedGeneticsHumansMetallothioneinRNA MessengerVector (molecular biology)Molecular BiologyTranscription factorGeneCells CulturedCytochrome P-450 CYP2C9biologyChemistryNuclear ProteinsCytochrome P450Oxidoreductases N-DemethylatingCell BiologyTransfectionMolecular biologyDNA-Binding ProteinsCytochrome P-450 CYP2B6C/EBPαCytochrome P-450 CYP2D6Steroid 16-alpha-HydroxylaseHepatocyte nuclear factor 4 alphaEnzyme InductionSteroid HydroxylasesCCAAT-Enhancer-Binding Proteinsbiology.proteinAryl Hydrocarbon HydroxylasesHuman hepatocyteCytochrome P450 gene regulationTranscription Factors
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Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

2015

Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed …

Genome instabilityRedox signalingRNA UntranslatedEpigenetic regulation of neurogenesisDNA RepairHuR mRNA-binding protein in the 3′-untranslated regionClinical BiochemistryHDAC histone deacetylaseReview ArticleAP-1 activator protein 1BiochemistryApe-1 apurinic/apyrimidinic endonuclease 1GPx-1 glutathione peroxidase-1Epigenesis GeneticHistonesTrx thioredoxinPHD prolylhydroxylaseBER base excision repairlcsh:QH301-705.5HO-1 heme oxygenase-1EpigenomicsGeneticsRegulation of gene expressionNox member of the NADPH oxidase familylcsh:R5-920JmjC Jumonji C domain-containing histone demethylasesHIF-1α hypoxia inducible factor-1α5-hmC 5-hydroxymethylcytosineddc:Cell biologyMMP matrix metalloproteinaseGrx glutaredoxinGAPDH glyceraldehyde-3-phosphate dehydrogenaseNrf2 nuclear factor erythroid related factor 2DNA methylationEpigeneticslcsh:Medicine (General)Oxidation-ReductionSignal Transduction5-mC 5-methylcytosineDNA repairDNA damageNF-κB nuclear factor-κBBiologyGenomic InstabilityRNS reactive nitrogen speciesROS reactive oxygen speciesNER nucleotide excision repairSOD superoxide dismutaseOxyR transcription factor (hydrogen peroxide-inducible genes activator)HumansEpigeneticsOrganic ChemistryPETN pentaerithrityl tetranitrateGene regulationOxidative StressDNMT DNA methyltransferaseGene Expression Regulationlcsh:Biology (General)AREs AU-rich elementsHAT histone acetyltransferaseKeap1 kelch-like ECH-associated protein 1BiomarkersCOPD chronic obstructive pulmonary disorderDNA DamageRedox Biology
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Neuronal Cell Nuclear Factor. A Nuclear Receptor Possibly Involved in the Control of Neurogenesis and Neuronal Differentiation

1997

We have cloned from a cDNA library of neuronal derivatives of retinoic-acid-induced embryonic carcinoma cells a nuclear receptor that may be involved in the control of late neurogenesis and early neuronal differentiation. The receptor which is practically identical in sequence with germ cell nuclear factor, has been designated neuronal cell nuclear factor (NCNF). NCNF is exclusively expressed in the neuronal derivatives of PCC7-Mz1 cells, with the expression beginning within hours of exposure to retinoic acid. In the developing mouse brain, NCNF is expressed in the marginal zones of the neuroepithelium which are known to contain young postmitotic neurons. NCNF binds to the DRO sequence ther…

Germ cell nuclear factorRetinoic acidReceptors Cytoplasmic and NuclearTretinoinBiologyLigandsBiochemistryMicechemistry.chemical_compoundNuclear Receptor Subfamily 6 Group A Member 1Tumor Cells CulturedAnimalsCloning MolecularReceptorIn Situ HybridizationNuclear receptor co-repressor 1NeuronsNeurogenesisBrainGene Expression Regulation DevelopmentalCell DifferentiationDNABlotting NorthernMolecular biologyDNA-Binding ProteinsRepressor ProteinsNeuroepithelial cellNuclear receptor coactivator 1Blotting SouthernOligodeoxyribonucleotidesnervous systemchemistryNuclear receptorEuropean Journal of Biochemistry
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The germ cell nuclear factor (GCNF)

2005

The germ cell nuclear factor (GCNF), which is also known as RTR (retinoid receptor-related testis-associated receptor) is a member of the nuclear receptor superfamily. As a natural ligand remains to be discovered, GCNF is referred to as an orphan receptor. Owing to GCNF's unique features and its distant relation to any other known nuclear receptor it has been classified as the only member of the subgroup six and designated NR6A1 by the Receptor Nomenclature Committee (Duarte et al., 2002: Nucleic Acids Res 30: 364-368). To date, GCNF has been cloned from distinct vertebrate species, including zebrafish, Xenopus laevis, mouse, rat, and human. Cloning and characterization of the gene, domain …

Germ cell nuclear factorXenopusEmbryonic DevelopmentReceptors Cytoplasmic and NuclearNuclear Receptor Subfamily 6 Group A Member 1GeneticsmedicineAnimalsHumansZebrafishGeneGeneticsOrphan receptorCloningbiologyGene Expression Regulation DevelopmentalCell DifferentiationCell Biologybiology.organism_classificationDNA-Binding ProteinsGerm Cellsmedicine.anatomical_structureNuclear receptorVertebratesGerm cellDevelopmental BiologyMolecular Reproduction and Development
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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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