Search results for "transactivation"

showing 10 items of 54 documents

Polycerasoidol, a Natural Prenylated Benzopyran with a Dual PPARα/PPARγ Agonist Activity and Anti-inflammatory Effect

2019

Dual peroxisome proliferator-activated receptor-α/γ (PPARα/γ) agonists regulate both lipid and glucose homeostasis under different metabolic conditions and can exert anti-inflammatory activity. We investigated the potential dual PPARα/γ agonism of prenylated benzopyrans polycerasoidol (1) and polycerasoidin (2) and their derivatives for novel drug development. Nine semisynthetic derivatives were prepared from the natural polycerasoidol (1) and polycerasoidin (2), which were evaluated for PPARα, -γ, -δ and retinoid X receptor-α activity in transactivation assays. Polycerasoidol (1) exhibited potent dual PPARα/γ agonism and low cytotoxicity. Structure–activity relationship studies revealed th…

Anti-Inflammatory AgentsRXRα/PPARγPharmaceutical ScienceRetinoid X receptorPharmacology01 natural sciencesAnalytical ChemistryStructure-Activity Relationshipchemistry.chemical_compoundTransactivationPrenylationPOLYCERASOIDOLDrug DiscoveryHumansStructure–activity relationshipGlucose homeostasisBenzopyransPPAR alphaMOLECULAR MODELINGCytotoxicityPrenylationPharmacologyMolecular Structure010405 organic chemistryChemistry[CHIM.ORGA]Chemical Sciences/Organic chemistryOrganic ChemistryCiencias QuímicasNATARUL PRODUCTSPeroxisome0104 chemical sciencesBenzopyranPPAR gamma010404 medicinal & biomolecular chemistryQuímica OrgánicaComplementary and alternative medicineMolecular MedicineCIENCIAS NATURALES Y EXACTAS
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The Peroxisomal 3-keto-acyl-CoA thiolase B Gene Expression Is under the Dual Control of PPARα and HNF4α in the Liver

2011

PPARα and HNF4α are nuclear receptors that control gene transcription by direct binding to specific nucleotide sequences. Using transgenic mice deficient for either PPARα or HNF4α, we show that the expression of the peroxisomal3-keto-acyl-CoA thiolase B(Thb) is under the dependence of these two transcription factors. Transactivation and gel shift experiments identified a novel PPAR response element within intron 3 of theThbgene, by which PPARα but not HNF4α transactivates. Intriguingly, we found that HNF4α enhanced PPARα/RXRα transactivation from TB PPRE3 in a DNA-binding independent manner. Coimmunoprecipitation assays supported the hypothesis that HNF4α was physically interacting with RXR…

Article SubjectResponse elementPeroxisome proliferator-activated receptorBiology03 medical and health sciencesTransactivation0302 clinical medicineDrug DiscoveryGene expression[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologySDV:BBMPharmacology (medical)[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologylcsh:QH301-705.5[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyTranscription factor030304 developmental biology[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismchemistry.chemical_classificationGeneticsEndocrinology and metabolism0303 health sciencesThiolaseIntron[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismCell biologylcsh:Biology (General)Nuclear receptorchemistry030220 oncology & carcinogenesisEndocrinologie et métabolismeResearch ArticlePPAR Research
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SOCS3 transactivation by PPARγ prevents IL-17-driven cancer growth.

2013

Abstract Activation of the transcription factor PPARγ by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARγ are incompletely characterized. Here, we identify the adapter-encoding gene SOCS3 as a critical transcriptional target of PPARγ. SOCS3 promoter binding and gene transactivation by PPARγ was associated with a repression in differentiation of proinflammatory T-helper (TH)17 cells. Accordingly, TH17 cells induced in vitro displayed increased SOCS3 expression and diminished capacity to produce interleukin (IL)-17 following activation of PPARγ by DHA. Furthermore, naïve CD4…

CD4-Positive T-LymphocytesCancer ResearchAngiogenesisMammary Neoplasms Experimental/genetics/pathology/prevention & controlSuppressor of Cytokine Signaling Proteinsddc:616.07BioinformaticsTransactivationMice0302 clinical medicineTumor Burden/drug effects/geneticsSOCS3Docosahexaenoic Acids/administration & dosage/pharmacologyPromoter Regions GeneticMice Knockout0303 health sciencesMice Inbred BALB CChemistryReverse Transcriptase Polymerase Chain ReactionInterleukin-17InterleukinCell DifferentiationCell biologyTumor BurdenOncology030220 oncology & carcinogenesisFemaleRNA InterferenceInterleukin 17Th17 Cells/drug effects/metabolismTranscriptional ActivationDocosahexaenoic AcidsBlotting WesternMice NudeCD4-Positive T-Lymphocytes/drug effects/metabolismProinflammatory cytokine03 medical and health sciencesSuppressor of Cytokine Signaling Proteins/genetics/metabolismCell Line TumorAnimalsTranscription factor030304 developmental biologyMammary Neoplasms ExperimentalPromoter Regions Genetic/geneticsDietMice Inbred C57BLPPAR gammaInterleukin-17/metabolismCell cultureSuppressor of Cytokine Signaling 3 ProteinCell Differentiation/drug effectsPPAR gamma/agonists/genetics/metabolismTh17 CellsCancer research
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β-Catenin Contributes to Lung Tumor Development Induced by EGFR Mutations

2014

Abstract The discovery of somatic mutations in EGFR and development of EGFR tyrosine kinase inhibitors (TKI) have revolutionized treatment for lung cancer. However, resistance to TKIs emerges in almost all patients and currently no effective treatment is available. Here, we show that β-catenin is essential for development of EGFR-mutated lung cancers. β-Catenin was upregulated and activated in EGFR-mutated cells. Mutant EGFR preferentially bound to and tyrosine phosphorylated β-catenin, leading to an increase in β-catenin–mediated transactivation, particularly in cells harboring the gefitinib/erlotinib-resistant gatekeeper EGFR-T790M mutation. Pharmacologic inhibition of β-catenin suppresse…

Cancer ResearchLung NeoplasmsCarcinogenesisAfatinibMutation MissenseAntineoplastic AgentsMice TransgenicAfatinibmedicine.disease_causeArticleTransactivationGefitinibCarcinoma Non-Small-Cell LungCell Line TumormedicineAnimalsHumansEpidermal growth factor receptorLung cancerbeta CateninMutationbiologyProtein Stabilitymedicine.diseaseXenograft Model Antitumor AssaysTumor BurdenUp-Regulationrespiratory tract diseasesErbB ReceptorsGene Expression Regulation NeoplasticHEK293 CellsOncologyDoxycyclineCateninImmunologyQuinazolinesCancer researchbiology.proteinCarcinogenesismedicine.drugCancer Research
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Androgen receptor activation by polychlorinated biphenyls

2013

The exposure to environmental endocrine disrupting compounds (EDC), as polychlorinated biphenyls (PCBs), widely diffused in the environment may produce epigenetic changes that affect the endocrine system. We found that PCBs activate AR transcriptional activity and that this effect is potentiated by the demethylase Jarid1b, a histone demethylase that catalyzes the removal of trimethylation of lysine 4 on histone H3 (H3K4me3), induced by PCB. The aim of the present study was to investigate the effect of the treatment of cultured cells (HEK293) with a mixture of the most diffused environmental PCBs and, also with dihydrotestosterone (DHT), on the functional interaction between AR and Jarid1b. …

Cancer ResearchbiologyCell biologyAndrogen receptorHistone H3TransactivationBiochemistryDihydrotestosteronebiology.proteinmedicineDemethylaseH3K4me3EpigeneticsJARID1BMolecular Biologymedicine.drugEpigenetics
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Oncogenic extracellular HSP70 disrupts the gap-junctional coupling between capillary cells

2015

// Dominique Thuringer 1 , Kevin Berthenet 1 , Laurent Cronier 2 , Gaetan Jego 1,3 , Eric Solary 4 , Carmen Garrido 1,3,5 1 INSERM, U866, Faculty of Medecine, Dijon, France 2 CNRS ERL7368, STIM Lab, University of Poitiers, Poitiers, France 3 University of Burgundy, Dijon, France 4 INSERM, U1009, Institut Gustave Roussy, Villejuif, France 5 CGFL, BP77980 21000 Dijon, France Correspondence to: Dominique Thuringer, email: // Keywords : HSP, Cx43, pannexin, Ca 2+ oscillations, ATP release Received : January 30, 2015 Accepted : February 17, 2015 Published : March 10, 2015 Abstract High levels of circulating heat shock protein 70 (HSP70) are detected in many cancers. In order to explore the effec…

Cell signalingPannexinBiologyMolecular biologyCx43Cell biologyATP releaseTransactivationCa2+ oscillationsOncologypannexinExtracellularbiology.proteinHSPPhosphorylationEpidermal growth factor receptorReceptorIntracellularResearch Paper
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Neuronal FGFR1 transactivation by inducing FGFR1/5-HT1A heteroreceptor complexes formation

2011

There are no clear data on the molecular mechanism by which the hippocampal 5-HT transmission contributes to the neuroprotective and antidepressant effects of 5-HT uptake blockers. Previously, we revealed that a 5-HT1A agonist may induce phosphorylation of FGFR1 and ERK1/2 in rat hippocampus independent of FGF-2, suggesting transactivation of FGFR1 tyrosine kinase in the absence of neurotrophic factor binding. As extension of previous work, using BRET analysis and coimmunoprecipitation in cellular models, FGFR1-5-HT1A heteroreceptor complexes have been demonstrated and agonist modulation characterized. In vitro assays on ERK1/2 phosphorylation in HEK cells and primary hippocampal cultures h…

FGFR1 5HT1A transactivation
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The cyclopentenone-type prostaglandin 15-deoxy-delta12,14-prostaglandin J2 inhibits CD95 ligand gene expression in T lymphocytes: interference with p…

2003

Abstract 15-Deoxy-Δ12,14-PGJ2 (15d-PGJ2) is a cyclopentenone-type PG endowed with anti-inflammatory properties and produced by different cells, including those of the immune system. 15d-PGJ2 is a natural ligand of the peroxisome proliferator-activated receptor (PPAR)-γ nuclear receptor, but relevant PPARγ-independent actions mediated by this prostanoid have been described. Fas (APO-1/CD95) and its ligand (Fas-L) are cell surface proteins whose interaction activates apoptosis of Fas-expressing targets. In T cells, the Fas-Fas-L system regulates activation-induced cell death and has been implicated in diseases in which lymphocyte homeostasis is compromised. Moreover, several studies have desc…

Fas Ligand ProteinNerve growth factor IBT-LymphocytesImmunologyPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearApoptosisCyclopentanesBiologyLigandsLymphocyte ActivationJurkat cellsImmediate-Early ProteinsTransactivationchemistry.chemical_compoundJurkat CellsMiceHeat Shock Transcription FactorsPeroxisomesImmunology and AllergyAnimalsHumansHSP70 Heat-Shock ProteinsGene Silencingfas ReceptorReceptorPromoter Regions GeneticCell Line TransformedEarly Growth Response Protein 1chemistry.chemical_classificationHybridomasMembrane GlycoproteinsProstaglandin D2Fas receptorMolecular biologyDNA-Binding ProteinschemistryNuclear receptorlipids (amino acids peptides and proteins)Prostaglandin D2Transcription Factors
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Oxidative stress induces the expression of the major histocompatibility complex in murine tumor cells.

2001

The effect of t-butyl hydroperoxide (t-BOOH) on the induction of the Major Histocompatibility Complex (MHC) class I genes has been studied in two cell clones (B9 and G2) of the methylcholanthrene-induced murine fibrosarcoma GR9. These two clones were selected based on their different biological and biochemical behavior specially related to their tumor induction capability when injected into a BALB/c mouse. t-BOOH (0.125 mM) induced the expression of H-2 molecules in both cell clones. In B9 cell clone, in which MHC basal expression is very low or absent, t-BOOH significantly induced H-2Kd, H-2Dd and H-2Ld molecules. In G2 cell clone the expression of MHC class I genes was also enhanced by th…

FibrosarcomaCellElectrophoretic Mobility Shift AssayBiologyMajor histocompatibility complexBiochemistryMajor Histocompatibility ComplexTransactivationMiceAntigentert-ButylhydroperoxideCell CloneMalondialdehydeMHC class ImedicineTumor Cells CulturedAnimalsGlutathione PeroxidaseMice Inbred BALB CSuperoxide DismutaseMHC Class I GeneHistocompatibility Antigens Class INF-kappa BDeoxyguanosineGeneral Medicine3T3 CellsCatalaseFlow CytometryMolecular biologyGlutathioneOxidative Stressmedicine.anatomical_structureGene Expression Regulation8-Hydroxy-2'-Deoxyguanosinebiology.proteinCD8MethylcholanthreneFree radical research
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Role for Tumor Necrosis Factor Alpha in Murine Cytomegalovirus Transcriptional Reactivation in Latently Infected Lungs

2004

ABSTRACT Interstitial pneumonia is a major clinical manifestation of primary or recurrent cytomegalovirus (CMV) infection in immunocompromised recipients of a bone marrow transplant. In a murine model, lungs were identified as a prominent site of CMV latency and recurrence. Pulmonary latency of murine CMV is characterized by high viral genome burden and a low incidence of variegated immediate-early (IE) gene expression, reflecting a sporadic activity of the major IE promoters (MIEPs) and enhancer. The enhancer-flanking promoters MIEP1/3 and MIEP2 are switched on and off during latency in a ratio of ∼2:1. MIEP1/3 latency-associated activity generates the IE1 transcript of the ie1/3 transcrip…

Gene Expression Regulation ViralHuman cytomegalovirusMuromegalovirusTranscription GeneticImmunologyBiologyMicrobiologyImmediate early proteinImmediate-Early ProteinsMiceViral ProteinsTransactivationVirologyGene expressionVirus latencymedicineAnimalsHumansEnhancerLungBone Marrow TransplantationMice Inbred BALB CTumor Necrosis Factor-alphaAlternative splicingPromoterHerpesviridae Infectionsmedicine.diseaseVirologyVirus LatencyVirus-Cell InteractionsDisease Models AnimalTransplantation IsogeneicInsect ScienceFemaleVirus ActivationJournal of Virology
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