Search results for "Transcriptional Activation"

showing 10 items of 102 documents

Adenoviral RB2/p130 gene transfer inhibits smooth muscle cell proliferation and prevents restenosis after angioplasty.

1999

Abstract —Smooth muscle cell (SMC) proliferation that results in neointima formation is implicated in the pathogenesis of atherosclerotic plaques and accounts for the high rates of restenosis that occur after percutaneous transluminal coronary angioplasty, a widespread treatment for coronary artery disease. Endothelial lesions trigger intense proliferative signals to the SMCs of the subintima, stimulating their reentry into the cell cycle from a resting G 0 state, resulting in neointima formation and vascular occlusion. Cellular proliferation is negatively controlled by growth-regulatory or tumor-suppressor genes, or both, such as the retinoblastoma gene family members ( RB/p105, p107, RB2…

NeointimaTranscriptional Activationmedicine.medical_specialtyPhysiologyadenovirus; cell cycle; gene therapy; p130; prb2; restenosisCellGenetic VectorsCell Cycle ProteinsPulmonary ArteryMuscle Smooth VascularAdenoviridaeCatheterizationPathogenesisRestenosisRecurrencemedicineAnimalsCarotid StenosisAngioplasty Balloon CoronaryGenes RetinoblastomaCells CulturedNeointimal hyperplasiaWound HealingRetinoblastoma-Like Protein p130business.industryCell growthGenetic transferCell CycleProteinsGenetic TherapyCell cyclemedicine.diseasePhosphoproteinsSurgeryE2F Transcription FactorsRatsDNA-Binding Proteinsmedicine.anatomical_structureCancer researchCardiology and Cardiovascular MedicinebusinessCarotid Artery InjuriesCarrier ProteinsTunica IntimaTranscription Factor DP1Cell DivisionRetinoblastoma-Binding Protein 1Transcription FactorsCirculation research
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The analysis of modified peroxisome proliferator responsive elements of the peroxisomal bifunctional enzyme in transfected HepG2 cells reveals two re…

1995

AbstractPeroxisome proliferators (PPs) are non-genotoxic carcinogens in rodents. They can induce the expression of numerous genes via the heterodimerization of two members of the steroid hormone receptor superfamily, called the peroxisome proliferator-activated receptor (PPAR) and the 9-cis retinoic acid receptor (RXR). Many of the PP responsive genes possess a peroxisome proliferator response element (PPRE) formed by two TGACCT-related motifs. The bifunctional enzyme (HD) PPRE contains 3 such motifs, creating DR1 and DR2 sequences. PPAR and RXR regulate transcription via the DR1 element while DR2 modulates the expression of the gene via auxiliary factors in HepG2 cells.

Peroxisome proliferator-activated receptor gammaReceptors Retinoic AcidSteroid hormone receptorMolecular Sequence DataResponse elementBiophysicsReceptors Cytoplasmic and NuclearPeroxisome proliferator-activated receptorchemical and pharmacologic phenomenaIn Vitro TechniquesRegulatory Sequences Nucleic AcidRetinoid X receptorBiologyPeroxisomal Bifunctional EnzymeTransfectionMicrobodiesBiochemistryGene Expression Regulation EnzymologicTranscriptional activationPeroxisomal Bifunctional EnzymeMultienzyme ComplexesStructural BiologyPeroxisome proliferator response element9-cis Retinoic acid receptor alphaTumor Cells CulturedGeneticsHumansRNA MessengerIsomerasesEnoyl-CoA HydrataseMolecular Biologychemistry.chemical_classificationBinding SitesBase Sequence3-Hydroxyacyl CoA DehydrogenasesPeroxisome proliferator-activated receptorCell BiologyDNA-Binding ProteinsRetinoic acid receptorRetinoid X ReceptorsLiverOligodeoxyribonucleotidesBiochemistrychemistryRat peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenaseEnzyme InductionPeroxisome proliferator-activated receptor alphaTranscription FactorsFEBS Letters
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Gata4 Blocks Somatic Cell Reprogramming By Directly Repressing Nanog

2012

Abstract Somatic cells can be reprogrammed to induced pluripotent stem (iPS) cells by ectopic expression of the four factors Oct4, Klf4, Sox2, and Myc. Here, we investigated the role of Gata4 in the reprogramming process and present evidence for a negative role of this family of transcription factors in the induction of pluripotency. Coexpression of Gata4 with Oct4, Klf4, and Sox2 with or without Myc in mouse embryonic fibroblasts greatly impaired reprogramming and endogenous Nanog expression. The lack of Nanog upregulation was associated with a blockade in the transition from the initiation phase of reprogramming to the full pluripotent state characteristic of iPS cells. Addition of Nanog …

Pluripotent Stem CellsTranscriptional ActivationHomeobox protein NANOGChromatin ImmunoprecipitationTranscription GeneticRex1Kruppel-Like Transcription FactorsDown-RegulationElectrophoretic Mobility Shift AssayBiologyCell LineProto-Oncogene Proteins c-mycKruppel-Like Factor 4MiceSOX2AnimalsRNA MessengerRNA Small InterferingInduced pluripotent stem cellEmbryonic Stem Cellsreproductive and urinary physiologyHomeodomain ProteinsSOXB1 Transcription FactorsNanog Homeobox ProteinCell DifferentiationNanog Homeobox ProteinCell BiologyCellular ReprogrammingEmbryonic stem cellGATA4 Transcription FactorKLF4embryonic structuresHepatocyte Nuclear Factor 3-betaCancer researchMolecular MedicineRNA Interferencebiological phenomena cell phenomena and immunityOctamer Transcription Factor-3ReprogrammingDevelopmental BiologyStem Cells
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Heat shock protein 27 is involved in SUMO-2/3 modification of heat shock factor 1 and thereby modulates the transcription factor activity

2009

Heat shock protein 27 (HSP27) accumulates in stressed cells and helps them to survive adverse conditions. We have already shown that HSP27 has a function in the ubiquitination process that is modulated by its oligomerization/phosphorylation status. Here, we show that HSP27 is also involved in protein sumoylation, a ubiquitination-related process. HSP27 increases the number of cell proteins modified by small ubiquitin-like modifier (SUMO)-2/3 but this effect shows some selectivity as it neither affects all proteins nor concerns SUMO-1. Moreover, no such alteration in SUMO-2/3 conjugation is achievable by another HSP, such as HSP70. Heat shock factor 1 (HSF1), a transcription factor responsib…

Protein sumoylationTranscriptional ActivationCancer Researchendocrine systemanimal structuresSUMO proteinHSP27 Heat-Shock ProteinsBiologyurologic and male genital diseasesenvironment and public healthSubstrate Specificity03 medical and health sciencesTransactivation0302 clinical medicineHeat Shock Transcription FactorsHeat shock proteinGeneticsAnimalsHumansAnimals Cell Nucleus/metabolism DNA-Binding Proteins/*metabolism HSP27 Heat-Shock Proteins/chemistry/*metabolism Hela Cells Humans Protein Multimerization Protein Structure[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyHSF1Protein Structure QuaternaryMolecular BiologyTranscription factorUbiquitinsHeat-Shock Proteins030304 developmental biologyCell Nucleus0303 health sciencesMolecular biologyHsp70Cell biologyHeat shock factorDNA-Binding ProteinsProtein TransportQuaternary Protein Transport Small Ubiquitin-Related Modifier Proteins/*metabolism Substrate Specificity Transcription Factors/*metabolism Transcriptional Activation Ubiquitins/*metabolism030220 oncology & carcinogenesisembryonic structuresSmall Ubiquitin-Related Modifier ProteinsProtein MultimerizationHeLa CellsMolecular ChaperonesTranscription Factors
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CD34+ progenitor to endothelial cell transition in post-pneumonectomy angiogenesis.

2012

In many species, pneumonectomy triggers compensatory lung growth that results in an increase not only in lung volume, but also in alveolar number. Whether the associated alveolar angiogenesis involves the contribution of blood-borne progenitor cells is unknown. To identify and characterize blood-borne progenitor cells contributing to lung growth after pneumonectomy in mice, we studied wild-type and wild-type/green fluorescence protein (GFP) parabiotic mice after left pneumonectomy. Within 21 days of pneumonectomy, a 3.2-fold increase occurred in the number of lung endothelial cells. This increase in total endothelial cells was temporally associated with a 7.3-fold increase in the number of …

Pulmonary and Respiratory MedicineTranscriptional ActivationPathologymedicine.medical_specialtyTime FactorsAngiogenesisCellular differentiationClinical BiochemistryGreen Fluorescent ProteinsCD34Neovascularization PhysiologicAntigens CD34Mice TransgenicBiologyMiceVasculogenesisCell MovementmedicineAnimalsRegenerationProgenitor cellPneumonectomyMolecular BiologyLungCell ProliferationStem CellsEndothelial CellsCell DifferentiationCell BiologyArticlesEndothelial stem cellVascular endothelial growth factor BMice Inbred C57BLGene Expression RegulationCancer researchStem cellAmerican journal of respiratory cell and molecular biology
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Requirement of Retinoic Acid Receptor Isotypes α, β, and γ during the Initial Steps of Neural Differentiation of PCC7 Cells

2005

Retinoic acid (RA) is indispensable for morphogenesis and differentiation of several tissues, including the nervous system. The requirement of the RA receptor (RAR) isotypes alpha, beta, and gamma and the putative role of retinoid X receptor-(RXR) signaling in RA-induced neural differentiation, was analyzed. For this compound-selective retinoids and the murine embryonal carcinoma cell line PCC7, a model system for RA-dependent neural differentiation was used. The present paper shows that proliferating PCC7 cells primarily express RXRalpha and RARalpha, lower levels of RXRbeta, and barely detectable amounts of RARbeta, RARgamma, and RXRgamma. At receptor-selective concentrations, only a RARa…

Receptors Retinoic AcidRetinoic acidReceptors Cytoplasmic and NuclearApoptosisLigandsMicechemistry.chemical_compoundEndocrinologyGenes ReporterNuclear Receptor Subfamily 6 Group A Member 1Protein IsoformsRetinoidReceptorGlutathione TransferaseNeuronsCell DeathReverse Transcriptase Polymerase Chain ReactionCell DifferentiationGeneral MedicineImmunohistochemistryUp-RegulationCell biologyDNA-Binding ProteinsBiochemistrySignal transductionPlasmidsProtein BindingSignal Transductionmedicine.drugTranscriptional ActivationDNA Complementarymedicine.drug_classRecombinant Fusion ProteinsBlotting WesternDown-RegulationTretinoinRetinoid X receptorBiologyTransfectionCell LineTretinoinCell Line TumormedicineAnimalsHumansMolecular BiologyCell ProliferationKineticsRetinoic acid receptorRetinoid X ReceptorschemistryNuclear receptorRNAOctamer Transcription Factor-3Transcription FactorsMolecular Endocrinology
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The induction of cytochrome P450 3A5 (CYP3A5) in the human liver and intestine is mediated by the xenobiotic sensors pregnane X receptor (PXR) and co…

2004

Induction of cytochrome P450 3A (CYP3A) by xenobiotics may lead to clinically relevant drug interactions. In contrast with other CYP3A family members, studies on the inducibility of CYP3A5 indicate conflicting results. We report the induction of CYP3A5 mRNA in 13 of 16 hepatocyte preparations exposed to rifampin. Furthermore, induction of CYP3A5 mRNA was observed in intestinal biopsies in three of eight probands following exposure to the antibiotic. The highest absolute levels of CYP3A5 transcripts were found following rifampin treatment in hepatocytes and intestines from carriers of CYP3A5*1 alleles. Elucidation of the mechanism involved in CYP3A5 induction revealed that constitutively act…

Receptors SteroidTime FactorsCYP3ABiopsyAmino Acid MotifsReceptors Cytoplasmic and NuclearPharmacology030226 pharmacology & pharmacyBiochemistryTransactivation0302 clinical medicineCytochrome P-450 Enzyme SystemGenes ReporterCytochrome P-450 CYP3AIntestinal MucosaReceptorPromoter Regions GeneticGenes Dominant0303 health sciencesPregnane X receptorPregnane X Receptor3. Good healthmedicine.anatomical_structureLiverHepatocyteRifampinPlasmidsProtein BindingTranscriptional ActivationHeterozygoteGenotypeBiologyTransfectionXenobiotics03 medical and health sciencesmedicineHumansRNA MessengerMolecular BiologyAllelesConstitutive Androstane Receptor030304 developmental biologyMessenger RNACYP3A4Cell BiologyMolecular biologyProtein Structure TertiaryHepatocytesRNADrug metabolismTranscription FactorsThe Journal of biological chemistry
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GAM/ZFp/ZNF512B is central to a gene sensor circuitry involving cell-cycle regulators, TGF beta effectors, Drosha and microRNAs with opposite oncogen…

2010

MicroRNAs (miRNAs) are small regulatory RNAs targeting multiple effectors of cell homeostasis and development, whose malfunctions are associated with major pathologies such as cancer. Herein we show that GAM/ZFp/ZNF512B works within an intricate gene regulatory network involving cell-cycle regulators, TGFβ effectors and oncogenic miRNAs of the miR-17-92 cluster. Thus, GAM impairs the transcriptional activation of the miR-17-92 promoter by c-Myc, downregulates miR-17-92 miRNAs differentially, and limits the activation of genes responsive to TGFβ canonical pathway. In contrast, TGFβ decreases GAM transcripts levels while differentially upregulating miR-17-92 miRNAs. In turn, miR-17, miR-20a a…

Ribonuclease IIITranscriptional ActivationRegulatorGene regulatory networkBiologyProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)Transforming Growth Factor betamicroRNAGeneticsE2F1HumansGene Regulatory NetworksDroshaFeedback PhysiologicalEffectorCell CycleTransforming growth factor betaCell cycleCell biologyMicroRNAsbiology.proteinCancer researchRNACarrier ProteinsE2F1 Transcription Factor
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Inhibition of VEGF expression through blockade of Hif1a and STAT3 signalling mediates the anti-angiogenic effect of melatonin in HepG2 liver cancer c…

2013

Background: Hepatocellular carcinoma (HCC) growth relies on angiogenesis via vascular endothelial growth factor (VEGF) release. Hypoxia within tumour environment leads to intracellular stabilisation of hypoxia inducible factor 1 alpha (Hif1α) and signal transducer and activator of transcription (STAT3). Melatonin induces apoptosis in HCC, and shows anti-angiogenic features in several tumours. In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate the anti-angiogenic effects of melatonin. Methods: HepG2 cells were treated with melatonin under normoxic or CoCl2-induced hypoxia. Gene expression was analysed by RT–qPCR and western blot. Melatonin-induced anti-…

STAT3 Transcription FactorTranscriptional ActivationVascular Endothelial Growth Factor ACancer ResearchCarcinoma HepatocellularTranscription GeneticAngiogenesisAngiogenesis InhibitorsApoptosismelatoninP300-CBP Transcription FactorsHif1αBiologyMelatoninSTAT3chemistry.chemical_compoundHypoxia-Inducible Factor 1-AlphamedicineHuman Umbilical Vein Endothelial CellsHumansp300-CBP Transcription FactorsSTAT3Promoter Regions GeneticTube formationNeovascularization PathologicLiver NeoplasmsCobaltHep G2 Cellshepatocellular carcinomaHypoxia-Inducible Factor 1 alpha SubunitVEGFCell Hypoxiadigestive system diseasesCyclic S-OxidesVascular endothelial growth factorGene Expression Regulation NeoplasticVascular endothelial growth factor AOncologychemistryCancer researchbiology.proteinTranslational Therapeuticsmedicine.drugSignal Transduction
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Epigenetic Regulation of Early- and Late-Response Genes in Acute Pancreatitis

2015

Abstract Chromatin remodeling seems to regulate the patterns of proinflammatory genes. Our aim was to provide new insights into the epigenetic mechanisms that control transcriptional activation of early- and late-response genes in initiation and development of severe acute pancreatitis as a model of acute inflammation. Chromatin changes were studied by chromatin immunoprecipitation analysis, nucleosome positioning, and determination of histone modifications in promoters of proinflammatory genes in vivo in the course of taurocholate-induced necrotizing pancreatitis in rats and in vitro in rat pancreatic AR42J acinar cells stimulated with taurocholate or TNF-α. Here we show that the upregulat…

Taurocholic AcidTranscriptional Activation0301 basic medicineChromatin ImmunoprecipitationImmunologyAcinar CellsBiologyMethylationChromatin remodelingEpigenesis GeneticHistones03 medical and health sciences0302 clinical medicineHistone methylationAnimalsImmunology and AllergyNucleosomeEpigeneticsPromoter Regions GeneticEarly Growth Response Protein 1Histone AcetyltransferasesInflammationPancreatitis Acute NecrotizingTumor Necrosis Factor-alphaDNA HelicasesNuclear ProteinsAcetylationHistone acetyltransferaseChromatin Assembly and DisassemblyRatsChromatin030104 developmental biologyHistoneGene Expression Regulation030220 oncology & carcinogenesisbiology.proteinCancer researchProtein Processing Post-TranslationalChromatin immunoprecipitationTranscription FactorsThe Journal of Immunology
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