Search results for "Coactivator"

showing 10 items of 52 documents

Mechanism of leptin expression in breast cancer cells: role of hypoxia-inducible factor-1α

2007

We reported previously that the obesity hormone leptin is overexpressed in breast cancer biopsies. Here, we investigated molecular mechanisms involved in this process, focusing on conditions that are associated with obesity, that is, hyperinsulinemia and induction of hypoxia. By using quantitative real-time PCR, immunofluorescent detection of proteins and enzyme-linked immunosorbent assays, we found that treatment of MCF-7 breast cancer cells with high doses of insulin or the hypoxia-mimetic agent CoCl2, or culturing the cells under hypoxic conditions significantly increased the expression of leptin mRNA and protein. Notably, the greatest leptin mRNA and protein expression were observed und…

Transcriptional ActivationCancer Researchmedicine.medical_specialtyActive Transport Cell NucleusBreast NeoplasmsBiologymedicine.disease_causeleptinbreast cancerInternal medicineCoactivatorGene expressionTumor Cells CulturedGeneticsmedicineHumansInsulinHIFp300-CBP Transcription FactorsPromoter Regions GeneticMolecular BiologyCell NucleusRegulation of gene expressionBinding SitesLeptin receptorLeptinPromoterCobaltHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaGene Expression Regulation NeoplasticEndocrinologyhyperinsulinemiaCarcinogenesisChromatin immunoprecipitationhormones hormone substitutes and hormone antagonistsProtein BindingOncogene
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Sex-based differences after a single bout of exercise on PGC1α isoforms in skeletal muscle: A pilot study

2020

To date, there are limited and incomplete data on possible sex-based differences in fiber-types of skeletal muscle and their response to physical exercise. Adult healthy male and female mice completed a single bout of endurance exercise to examine the sex-based differences of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α), heat shock protein 60 (Hsp60), interleukin 6 (IL-6) expression, as well as the Myosin Heavy Chain (MHC) fiber-type distribution in soleus and extensor digitorum longus (EDL) muscles. Our results showed for the first time that in male soleus, a muscle rich of type IIa fibers, endurance exercise activates specifically genes involved in mito…

0301 basic medicineMalemedicine.medical_specialtyAlpha (ethology)interleukin 6Physical exerciseMotor ActivityBiochemistryMitochondrial Proteins03 medical and health sciencesMice0302 clinical medicineSex FactorsEndurance trainingphysical exerciseInternal medicineHeat shock proteinMyosinGeneticsmedicineAnimalsProtein Isoformsskeletal muscleInterleukin 6Muscle SkeletalMolecular BiologyMice Inbred BALB Cbiologybusiness.industryInterleukin-6Myosin Heavy ChainSkeletal muscleChaperonin 60musculoskeletal systemPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha030104 developmental biologyEndocrinologymedicine.anatomical_structureMitochondrial biogenesisbiology.proteinFemalebusiness030217 neurology & neurosurgeryheat shock protein 60Biotechnology
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Underexpressed Coactivators PGC1α AND SRC1 Impair Hepatocyte Nuclear Factor 4α Function and Promote Dedifferentiation in Human Hepatoma Cells

2006

Hepatocyte nuclear factor 4alpha (HNF4alpha) plays critical roles during liver development and in the transcriptional regulation of many hepatic genes in adult liver. Here we have demonstrated that in human hepatoma HepG2 cells, HNF4alpha is expressed at levels as high as in human liver but its activity on target genes is very low or absent. We have discovered that the low expression of key coactivators (PGC1alpha, SRC1, SRC2, and PCAF) might account for the lack of function of HNF4alpha in HepG2 cells. Among them, PGC1alpha and SRC1 are the two most important HNF4alpha coactivators as revealed by reporter assays with an Apo-CIII promoter construct. Moreover, the expression of these two coa…

AdultMalemedicine.medical_specialtyCarcinoma HepatocellularDown-RegulationBiologyBiochemistryNuclear Receptor Coactivator 1Cell Line TumorInternal medicinemedicineTranscriptional regulationHomeostasisHumansMolecular BiologyPsychological repressionHeat-Shock ProteinsAgedHistone AcetyltransferasesLiver NeoplasmsCell DifferentiationCell BiologyMiddle AgedPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhenotypeCell biologyNuclear receptor coactivator 1Hepatocyte nuclear factorsEndocrinologyHepatocyte Nuclear Factor 4LiverPCAFCell cultureFemaleHomeostasisTranscription FactorsJournal of Biological Chemistry
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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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Co-regulator recruitment and the mechanism of retinoic acid receptor synergy.

2002

Crystal structure and co-regulator interaction studies have led to a general mechanistic view of the initial steps of nuclear receptor (NR) action. Agonist-induced transconformation of the ligand-binding domain (holo-LBD) leads to the formation of co-activator complexes, and destabilizes the co-repressor complexes bound to the ligand-free (apo) LBD. However, the molecular basis of retinoid-X receptor (RXR) 'subordination' in heterodimers, an essential mechanism to avoid signalling pathway promiscuity, has remained elusive. RXR, in contrast to its heterodimer partner, cannot autonomously induce transcription on binding of cognate agonists. Here we show that RXR can bind ligand and recruit co…

Protein ConformationReceptors Retinoic AcidPlasma protein bindingRetinoid X receptorLigandsNuclear Receptor Coactivator 2Structure-Activity RelationshipmedicineNuclear Receptor Co-Repressor 2Binding siteNuclear receptor co-repressor 2PhysicsMultidisciplinaryCell biologyDNA-Binding ProteinsRepressor ProteinsRetinoic acid receptorRetinoid X ReceptorsMechanism of actionBiochemistryNuclear receptorModels Chemicalembryonic structuresNuclear receptor coactivator 2medicine.symptomDimerizationProtein BindingTranscription FactorsNature
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YAP/TAZ activity in stromal cells prevents ageing by controlling cGAS-STING

2022

Ageing is intimately connected to the induction of cell senescence(1,2), but why this is so remains poorly understood. A key challenge isthe identification of pathways that normally suppress senescence, are lost during ageing and are functionally relevant to oppose ageing(3). Here we connected the structural and functional decline of ageing tissues to attenuated function of the master effectors of cellular mechanosignalling YAP and TAZ. YAP/TAZ activity declines during physiological ageing in stromal cells, and mimicking such decline through genetic inactivation of YAP/TAZ in these cells leads to accelerated ageing. Conversely, sustaining YAP function rejuvenates old cells and opposes the e…

AgingMechanotransductionActin-Related Protein 2; Cellular Senescence; Extracellular Matrix; Healthy Aging; Immunity Innate; Lamin Type B; Mechanotransduction Cellular; Nuclear Envelope; Signal Transduction; Aging; Membrane Proteins; Nucleotidyltransferases; Stromal Cells; Transcriptional Coactivator with PDZ-Binding Motif Proteins; YAP-Signaling ProteinsNuclear EnvelopeSettore MED/08 - Anatomia PatologicaYAP TAZ ageing C-GAS STINGMechanotransduction CellularArticleHealthy AgingInnateCellular SenescenceAdaptor Proteins Signal TransducingMultidisciplinaryLamin Type BImmunityMembrane ProteinsYAP-Signaling ProteinsPhosphoproteinsNucleotidyltransferasesImmunity InnateExtracellular MatrixTranscriptional Coactivator with PDZ-Binding Motif ProteinsActin-Related Protein 2CellularStromal CellsSignal Transduction
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TAZ is required for metastatic activity and chemoresistance of breast cancer stem cells

2015

Metastatic growth in breast cancer (BC) has been proposed as an exclusive property of cancer stem cells (CSCs). However, formal proof of their identity as cells of origin of recurrences at distant sites and the molecular events that may contribute to tumor cell dissemination and metastasis development are yet to be elucidated. In this study, we analyzed a set of patient-derived breast cancer stem cell (BCSC) lines. We found that in vitro BCSCs exhibit a higher chemoresistance and migratory potential when compared with differentiated, nontumorigenic, breast cancer cells (dBCCs). By developing an in vivo metastatic model simulating the disease of patients with early BC, we observed that BCSCs…

cancer stem cellsTAZAnimals; Biomarkers Tumor; Breast Neoplasms; Cell Line Tumor; Disease-Free Survival; Female; Gene Expression Regulation Neoplastic; Humans; Mice; Neoplasm Metastasis; Neoplasm Recurrence Local; Neoplastic Stem Cells; Transcription Factors; Xenograft Model Antitumor AssaysCancer ResearchBioinformaticschemotherapyMetastasistaz; breast cancerMiceNeoplasm Metastasiseducation.field_of_studyTumorIntracellular Signaling Peptides and ProteinsCell cycleGene Expression Regulation NeoplasticLocalNeoplastic Stem Cellsbreast cancer; cancer stem cells; chemotherapy; metastasis; TAZ; Animals; Biomarkers Tumor; Breast Neoplasms; Cell Line Tumor; Disease-Free Survival; Female; Gene Expression Regulation Neoplastic; Humans; Intracellular Signaling Peptides and Proteins; Mice; Neoplasm Metastasis; Neoplasm Recurrence Local; Neoplastic Stem Cells; Xenograft Model Antitumor Assays; Molecular Biology; Genetics; Cancer ResearchFemaleStem cellPopulationBreast NeoplasmsBiologyDisease-Free SurvivalCell Linebreast cancer cancer stem cells TAZBreast cancerbreast cancerCancer stem cellSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicineBiomarkers TumorGeneticsmetastasisAnimalsHumanseducationMolecular BiologyHippo signaling pathwayNeoplasticCancermedicine.diseaseXenograft Model Antitumor AssaysNeoplasm RecurrenceGene Expression RegulationTranscriptional Coactivator with PDZ-Binding Motif ProteinsCancer researchTrans-ActivatorsNeoplasm Recurrence LocalBiomarkersTranscription Factors
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The estrogen receptor α:insulin receptor substrate 1 complex in breast cancer: structure–function relationships

2007

Background: Insulin receptor substrate 1 (IRS-1) is a signaling molecule that exerts a key role in mediating cross talk between estrogen receptor a (ERa) and insulin-like growth factor 1 (IGF-1) in breast cancer cells. Previously, we demonstrated that a fraction of IRS-1 binds ERa, translocates to the nucleus, and modulates ERa-dependent transcription at estrogen response elements (ERE). Here, we studied structure-function relationships of the ER-a:IRS-1 complex under IGF-1 and/or estradiol (E 2 ) stimulation. Materials and methods: ERa and IRS-1 deletion mutants were used to analyze structural and functional ERα/IRS-1 interactions. IRS-1 binding to ERE and IRS-1 role in ERa-dependent ERE t…

medicine.medical_specialtyInsulin Receptor Substrate ProteinsActive Transport Cell NucleusEstrogen receptorRepressorBreast NeoplasmsBiologyStructure-Activity Relationshipestrogen receptor alpha (ERa) Insulin receptor substrate 1 (IRS-1) breast cancerCell Line TumorInternal medicineCoactivatormedicineHumansInsulin-Like Growth Factor IReceptors InterferonEstradiolEstrogen Receptor alphaHematologyDNA-binding domainPhosphoproteinsPeptide FragmentsReceptor InsulinProtein Structure TertiaryCell biologyIRS1Repressor ProteinsPleckstrin homology domainEndocrinologyOncologyInsulin Receptor Substrate ProteinsFemaleChromatin immunoprecipitationProtein BindingAnnals of Oncology
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Effects of Conjugated Linoleic Acid Associated With Endurance Exercise on Muscle Fibres and Peroxisome Proliferator-Activated Receptor γ Coactivator …

2016

Conjugated linoleic acid (CLA) has been reported to improve muscle hypertrophy, steroidogenesis, physical activity, and endurance capacity in mice, although the molecular mechanisms of its actions are not completely understood. The aim of the present study was to identify whether CLA alters the expression of any of the peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) isoforms, and to evaluate the possible existence of fibre-type-specific hypertrophy in the gastrocnemius and plantaris muscles. Mice were randomly assigned to one of four groups: placebo sedentary, CLA sedentary, placebo trained, or CLA trained. The CLA groups were gavaged with 35 μl per day of Tonalin® FFA 8…

MaleConjugatedPhysiologyClinical BiochemistryMuscle Fibers SkeletalMuscle FibersMiceLectinsPhysical Conditioning AnimalAnimalsProtein IsoformsLinoleic Acids ConjugatedInbred BALB CMice Inbred BALB CAnimalSettore BIO/16 - Anatomia UmanaAdenylate KinaseSkeletalCell BiologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhysical ConditioningHindlimbMitochondriaLinoleic AcidsAdenylate Kinase; Animals; Dietary Supplements; Hindlimb; Lectins; Linoleic Acids Conjugated; Male; Mice Inbred BALB C; Mitochondria; Muscle Fibers Skeletal; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Protein Isoforms; Physical Conditioning Animal; Physiology; Clinical Biochemistry; Cell BiologyDietary SupplementsFat supplements
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Nuclear receptors modulate the interaction of Sp1 and GC-rich DNA via ternary complex formation

2000

Binding sites for transcription factor Sp1have been implicated in the transcriptional regulation of several genes by hormones or vitamins, and here we show that a GC-rich element contributes to the retinoic acid response of the interleukin 1β promoter. To explain such observations, it has been proposed that nuclear receptors can interact with Sp1 bound to GC-rich DNA. However, evidence supporting this model has remained indirect. So far, nuclear receptors have not been detected in a complex with Sp1 and GC-rich DNA, and the expected ternary complexes in non-denaturing gels were not seen. In search for these missing links we found that nuclear receptors [retinoic acid receptor (RAR), thyroid…

Cell ExtractsTranscriptional ActivationReceptors Retinoic AcidSp1 Transcription FactorRecombinant Fusion ProteinsReceptors Cytoplasmic and NuclearTretinoinRetinoic acid receptor betaBiologyRetinoid X receptorLigandsResponse ElementsTransfectionModels BiologicalBiochemistryAntibodiesCell LineSubstrate SpecificityAnimalsPromoter Regions GeneticMolecular BiologyNuclear receptor co-repressor 1Nuclear receptor co-repressor 2Binding SitesReceptors Thyroid HormoneDNACell BiologyRetinoic acid receptor gammaRetinoid X receptor gammaGC Rich SequenceProtein Structure TertiaryNuclear receptor coactivator 1Retinoic acid receptorDrosophila melanogasterEcdysteroneRetinoid X ReceptorsOligodeoxyribonucleotidesBiochemistryReceptors CalcitriolThermodynamicsResearch ArticleInterleukin-1Protein BindingTranscription FactorsBiochemical Journal
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