Search results for "MICE"

showing 10 items of 6027 documents

An epistatic mini-circuitry between the transcription factors Snail and HNF4α controls liver stem cell and hepatocyte features exhorting opposite reg…

2011

Preservation of the epithelial state involves the stable repression of epithelial-to-mesenchymal transition program, whereas maintenance of the stem compartment requires the inhibition of differentiation processes. A simple and direct molecular mini-circuitry between master elements of these biological processes might provide the best device to keep balanced such complex phenomena. In this work, we show that in hepatic stem cell Snail, a transcriptional repressor of the hepatocyte differentiation master gene HNF4α, directly represses the expression of the epithelial microRNAs (miRs)-200c and-34a, which in turn target several stem cell genes. Notably, in differentiated hepatocytes HNF4α, p…

Transcription GeneticTranscription FactorCellular differentiationLiver Stem CellSnailMESH: Mice KnockoutMESH: HepatocytesMice0302 clinical medicineSnail; hnf4a; mir-200; mir-34a; stemness; hepatocyte differentiationHepatocyteMESH: AnimalsMice KnockoutHepatocyte differentiationmir-34a0303 health sciencesStemneStem CellsMicroRNACell DifferentiationMESH: Transcription FactorsCell biologySnailmir-200Hepatocyte Nuclear Factor 4Liver030220 oncology & carcinogenesisMiRs-200MESH: Hepatocyte Nuclear Factor 4Hepatocyte differentiation; HNF4a; MiR-34a; MiRs-200; Snail; Stemness; Animals; Cell Differentiation; Epithelial-Mesenchymal Transition; Hepatocyte Nuclear Factor 4; Hepatocytes; Liver; Mice; Mice Knockout; MicroRNAs; Snail Family Transcription Factors; Stem Cells; Transcription Factors; Transcription Genetic; Cell Biology; Molecular BiologyStem cellhnf4aMESH: Cell Differentiationhepatocyte differentiationEpithelial-Mesenchymal TransitionMESH: Stem Cells[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologystemness03 medical and health sciencesStem Cellbiology.animalAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEpithelial–mesenchymal transitionMESH: MiceMolecular BiologyTranscription factor030304 developmental biologyOriginal PaperAnimalMESH: Transcription GeneticSnail Family Transcription FactorCell BiologyMolecular biologyMicroRNAsMESH: Epithelial-Mesenchymal TransitionHepatocyte nuclear factor 4HepatocytesSnail Family Transcription FactorsMESH: MicroRNAsMESH: LiverTranscription FactorsCell Death & Differentiation
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Recruitment of HIF-1α and HIF-2α to common target genes is differentially regulated in neuroblastoma: HIF-2α promotes an aggressive phenotype

2006

In neuroblastoma specimens, HIF-2alpha but not HIF-1alpha is strongly expressed in well-vascularized areas. In vitro, HIF-2alpha protein was stabilized at 5% O2 (resembling end capillary oxygen conditions) and, in contrast to the low HIF-1alpha activity at this oxygen level, actively transcribed genes like VEGF. Under hypoxia (1% O2), HIF-1alpha was transiently stabilized and primarily mediated acute responses, whereas HIF-2alpha protein gradually accumulated and governed prolonged hypoxic gene activation. Knockdown of HIF-2alpha reduced growth of neuroblastoma tumors in athymic mice. Furthermore, high HIF-2alpha protein levels were correlated with advanced clinical stage and high VEGF expr…

Transcriptional ActivationCancer ResearchProcollagen-Proline DioxygenaseAggressive phenotypeCELLCYCLEBiologyMiceNeuroblastomaNeuroblastomaBasic Helix-Loop-Helix Transcription FactorsTumor Cells CulturedmedicineAnimalsHumansRNA MessengerChildHypoxiaGeneOligonucleotide Array Sequence AnalysisRegulation of gene expressionGene knockdownGene Expression ProfilingCell BiologyCell cycleHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseIn vitroGene Expression Regulation NeoplasticOxygenPhenotypeOncologyImmunologyCancer researchFemalemedicine.symptomNeoplasm TransplantationCancer Cell
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The HMGA1 protoncogene frequently deregulated in cancer is a transcriptional target of E2F1

2011

Reactivation of the HMGA1 protoncogene is very frequent in human cancer, but still very little is known on the molecular mechanisms leading to this event. Prompted by the finding of putative E2F binding sites in the human HMGA1 promoter and by the frequent deregulation of the RB/E2F1 pathway in human carcinogenesis, we investigated whether E2F1 might contribute to the regulation of HMGA1 gene expression. Here we report that E2F1 induces HMGA1 by interacting with a 193bp region of the HMGA1 promoter containing an E2F binding site surrounded by three putative Sp1 binding sites. Both gain and loss of function experiments indicate that Sp1 functionally interacts with E2F1 to promote HMGA1 expre…

Transcriptional ActivationChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternMolecular Sequence DataReal-Time Polymerase Chain ReactionRetinoblastoma ProteinSp1MiceAnimalsHumansPituitary NeoplasmsThyroid NeoplasmsHMGA1a ProteinPituitary NeoplasmRNA MessengerPromoter Regions GeneticCarcinogenesiThyroid NeoplasmHMGA1 promoterMice KnockoutBinding SitesBase SequenceAnimalReverse Transcriptase Polymerase Chain ReactionBinding SiteMutationMutagenesis Site-DirectedTranscriptionE2F1 Transcription FactorHumansp1; carcinogenesis; hmga1 promoter; transcription
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Epigenetic activation of a cryptic TBC1D16 transcript enhances melanoma progression by targeting EGFR

2015

Metastasis is respoMetastasis is responsible for most cancer-related deaths, and, among common tumor types, melanoma is one with great potential to metastasize. Here we study the contribution of epigenetic changes to the dissemination process by analyzing the changes that occur at the DNA methylation level between primary cancer cells and metastases. We found a hypomethylation event that reactivates a cryptic transcript of the Rab GTPase activating protein TBC1D16 (TBC1D16-47 kDa; referred to hereafter as TBC1D16-47KD) to be a characteristic feature of the metastatic cascade. This short isoform of TBC1D16 exacerbates melanoma growth and metastasis both in vitro and in vivo. By combining imm…

Transcriptional ActivationGTPase-activating proteinImmunoprecipitationMice NudeEditorials: Cell Cycle FeaturesBiologyBioinformaticsMethylationGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticMetastasisMetastasisEpigènesiMetàstasiCell Line TumormedicineAnimalsImmunoprecipitationProtein IsoformsRNA MessengerEpigeneticsNeoplasm MetastasisRNA Small InterferingPromoter Regions GeneticProteïnes supressores de tumorsProtein Kinase InhibitorsMelanomaMelanomaGTPase-Activating ProteinsGeneral MedicineMethylationDNA MethylationPrognosismedicine.diseaseTumor suppressor proteinErbB ReceptorsMolecular WeightTreatment Outcomerab GTP-Binding ProteinsDNA methylationDisease ProgressionCancer researchRabMetilacióProtein BindingSignal TransductionEpigenesisNature Medicine
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Peroxisome-proliferator-activated receptors as physiological sensors of fatty acid metabolism: molecular regulation in peroxisomes

2001

The enzymes required for the beta-oxidation of fatty acyl-CoA are present in peroxisomes and mitochondria. Administration of hypolipidaemic compounds such as clofibrate to rodents leads to an increase in the volume and density of peroxisomes in liver cells. These proliferators also induce simultaneously the expression of genes encoding acyl-CoA oxidase, enoyl-CoA hydratase-hydroxyacyl-CoA dehydrogenase (multifunctional enzyme) and thiolase (3-ketoacyl-CoA thiolase). All these enzymes are responsible for long-chain and very-long-chain fatty acid beta-oxidation in peroxisomes. Similar results were observed when rat hepatocytes, or liver-derived cell lines, were cultured with a peroxisome prol…

Transcriptional ActivationGuinea PigsResponse elementReceptors Cytoplasmic and NuclearBiologyBiochemistryGene Expression Regulation EnzymologicMicechemistry.chemical_compoundPeroxisomesAnimalsAcetyl-CoA C-AcetyltransferasePhosphorylationTranscription factorProtein Kinase Cchemistry.chemical_classificationFatty acid metabolismThiolaseFatty AcidsFatty acidPeroxisomeRatsLiverchemistryBiochemistryAcetyl-CoA C-acetyltransferasePeroxisome proliferator-activated receptor alphaSignal TransductionTranscription FactorsBiochemical Society Transactions
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The Streptococcal Exotoxin Streptolysin O Activates Mast Cells To Produce Tumor Necrosis Factor Alpha by p38 Mitogen-Activated Protein Kinase- and Pr…

2003

ABSTRACTStreptolysin O (SLO), a major virulence factor of pyogenic streptococci, binds to cholesterol in the membranes of eukaryotic cells and oligomerizes to form large transmembrane pores. While high toxin doses are rapidly cytocidal, low doses are tolerated because a limited number of lesions can be resealed. Here, we report that at sublethal doses, SLO activates primary murine bone marrow-derived mast cells to degranulate and to rapidly induce or enhance the production of several cytokine mRNAs, including tumor necrosis factor alpha (TNF-α). Mast cell-derived TNF-α plays an important protective role in murine models of acute inflammation, and the production of this cytokine was analyzed…

Transcriptional ActivationImmunologyBiologyp38 Mitogen-Activated Protein KinasesMicrobiologyMiceBacterial ProteinsmedicineAnimalsASK1Mast CellsRNA MessengerProtein kinase AProtein Kinase CProtein kinase CMice Inbred BALB CDose-Response Relationship DrugTumor Necrosis Factor-alphaMast cellMolecular PathogenesisProtein kinase RMolecular biologyInterleukin 33Infectious Diseasesmedicine.anatomical_structureStreptolysinsParasitologyTumor necrosis factor alphaStreptolysinMitogen-Activated Protein KinasesInfection and Immunity
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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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CD8 T Cells Control Cytomegalovirus Latency by Epitope-Specific Sensing of Transcriptional Reactivation

2006

ABSTRACT During murine cytomegalovirus (mCMV) latency in the lungs, most of the viral genomes are transcriptionally silent at the major immediate-early locus, but rare and stochastic episodes of desilencing lead to the expression of IE1 transcripts. This low-frequency but perpetual expression is accompanied by an activation of lung-resident effector-memory CD8 T cells specific for the antigenic peptide 168-YPHFMPTNL-176, which is derivedfrom the IE1 protein. These molecular and immunological findings were combined in the “silencing/desilencing and immune sensing hypothesis” of cytomegalovirus latency and reactivation. This hypothesis proposes that IE1 gene expression proceeds to cell surfac…

Transcriptional ActivationMuromegalovirusvirusesImmunologyAntigen presentationCD8-Positive T-LymphocytesVirus ReplicationMajor histocompatibility complexModels BiologicalMicrobiologyEpitopeImmediate-Early ProteinsEpitopesImmunocompromised HostMiceAntigenVirologyMHC class IVirus latencymedicineAnimalsGene silencingCytotoxic T cellAmino Acid SequenceAntigens ViralLungBone Marrow TransplantationMice Inbred BALB CBase Sequencebiologyvirus diseasesHerpesviridae Infectionsbiochemical phenomena metabolism and nutritionmedicine.diseaseVirologyMolecular biologyVirus LatencyVirus-Cell InteractionsPhenotypeAmino Acid SubstitutionInsect ScienceDNA ViralMutagenesis Site-DirectedTrans-Activatorsbiology.proteinFemaleJournal of Virology
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Transactivation of cellular genes involved in nucleotide metabolism by the regulatory IE1 protein of murine cytomegalovirus is not critical for viral…

2008

ABSTRACT Despite its high coding capacity, murine CMV (mCMV) does not encode functional enzymes for nucleotide biosynthesis. It thus depends on cellular enzymes, such as ribonucleotide reductase (RNR) and thymidylate synthase (TS), to be supplied with deoxynucleoside triphosphates (dNTPs) for its DNA replication. Viral transactivation of these cellular genes in quiescent cells of host tissues is therefore a parameter of viral fitness relevant to pathogenicity. Previous work has shown that the IE1, but not the IE3, protein of mCMV transactivates RNR and TS gene promoters and has revealed an in vivo attenuation of the mutant virus mCMV-ΔIE1. It was attractive to propose the hypothesis that la…

Transcriptional ActivationMuromegalovirusvirusesImmunologyMutantMolecular Sequence DataBiologyVirus ReplicationMicrobiologyImmediate-Early ProteinsTransactivationMiceVirologyAnimalsPoint MutationAmino Acid SequencePromoter Regions GeneticGeneCells CulturedRegulation of gene expressionMice Inbred BALB CBase SequenceNucleotidesDNA replicationvirus diseasesTransfectionbiochemical phenomena metabolism and nutritionFibroblastsMolecular biologyGenome Replication and Regulation of Viral Gene ExpressionRibonucleotide reductaseViral replicationGene Expression RegulationLiverInsect ScienceNIH 3T3 CellsPeptidesSequence AlignmentJournal of virology
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Reduction of Cardiac Fibrosis by Interference With YAP-Dependent Transactivation

2022

Background: Conversion of cardiac stromal cells into myofibroblasts is typically associated with hypoxia conditions, metabolic insults, and/or inflammation, all of which are predisposing factors to cardiac fibrosis and heart failure. We hypothesized that this conversion could be also mediated by response of these cells to mechanical cues through activation of the Hippo transcriptional pathway. The objective of the present study was to assess the role of cellular/nuclear straining forces acting in myofibroblast differentiation of cardiac stromal cells under the control of YAP (yes-associated protein) transcription factor and to validate this finding using a pharmacological agent that interf…

Transcriptional ActivationPhysiologyfibrosismyofibroblastsVerteporfinheart failureYAP-Signaling ProteinsSettore MED/11 - Malattie dell'Apparato CardiovascolareSettore MED/23 - Chirurgia Cardiacafibrosis; heart failure; myofibroblasts; stromal cell; transcription factorsstromal cellPhosphoproteinscell mechanics; fibrosis; heart failure; myofibroblasts; stromal cell; YAP transcription factor;MiceYAP transcription factorcell mechanicsSettore CHIM/09 - Farmaceutico Tecnologico Applicativotranscription factorsTrans-ActivatorsAnimalsHumansCardiology and Cardiovascular MedicineAdaptor Proteins Signal Transducing
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