Search results for "Enhancer Elements"

showing 10 items of 35 documents

Prox1 Is Required for Oligodendrocyte Cell Identity in Adult Neural Stem Cells of the Subventricular Zone

2016

Abstract Adult neural stem cells with the ability to generate neurons and glia cells are active throughout life in both the dentate gyrus (DG) and the subventricular zone (SVZ). Differentiation of adult neural stem cells is induced by cell fate determinants like the transcription factor Prox1. Evidence has been provided for a function of Prox1 as an inducer of neuronal differentiation within the DG. We now show that within the SVZ Prox1 induces differentiation into oligodendrocytes. Moreover, we find that loss of Prox1 expression in vivo reduces cell migration into the corpus callosum, where the few Prox1 deficient SVZ-derived remaining cells fail to differentiate into oligodendrocytes. Thu…

0301 basic medicineAdult neurogenesisMice0302 clinical medicineNeural Stem CellsCell MovementLateral VentriclesPromoter Regions GeneticCells CulturedMOUSE-BRAINReceptors NotchOligodendrocytesNeurogenesisCell DifferentiationLINEAGEAnatomyOlfactory BulbNeural stem cellCell biologyNeuroepithelial cellAdult Stem CellsOligodendrogliaDIFFERENTIATIONEnhancer Elements Geneticmedicine.anatomical_structureGene Knockdown TechniquesMolecular MedicineSPINAL-CORDStem cellSUBCELLULAR-LOCALIZATIONProtein BindingAdult stem cellOLIG2NeurogenesisSubventricular zoneBiology03 medical and health sciencesNeurosphereProx1medicineAnimalsCell LineageOLFACTORY-BULBBody PatterningHomeodomain ProteinsTumor Suppressor ProteinsCell BiologyMAMMALIAN BRAINOligodendrocyte Transcription Factor 2030104 developmental biologyNeuropoiesisPROGENITOR CELLSGene Expression Regulationnervous system030217 neurology & neurosurgeryDevelopmental BiologyStem Cells
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MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
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An Intronic cis-Regulatory Element Is Crucial for the Alpha Tubulin Pl-Tuba1a Gene Activation in the Ciliary Band and Animal Pole Neurogenic Domains …

2017

In sea urchin development, structures derived from neurogenic territory control the swimming and feeding responses of the pluteus as well as the process of metamorphosis. We have previously isolated an alpha tubulin family member of Paracentrotus lividus (Pl-Tuba1a, formerly known as Pl-Talpha2) that is specifically expressed in the ciliary band and animal pole neurogenic domains of the sea urchin embryo. In order to identify cis-regulatory elements controlling its spatio-temporal expression, we conducted gene transfer experiments, transgene deletions and site specific mutagenesis. Thus, a genomic region of about 2.6 Kb of Pl-Tuba1a, containing four Interspecifically Conserved Regions (ICRs…

0301 basic medicineEmbryologyPolarity in embryogenesislcsh:MedicineGene ExpressionMedicine (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)medicine.disease_causeBiochemistryTubulinGene expressionElectron MicroscopyTransgeneslcsh:SciencePromoter Regions GeneticSea urchinConserved SequenceSequence DeletionGeneticsRegulation of gene expressionMicroscopyMutationMultidisciplinaryMedicine (all)Gene Expression Regulation DevelopmentalGenomicsAnimal ModelsTATA BoxEnzymesEnhancer Elements GeneticExperimental Organism Systemsembryonic structuresParacentrotusTranscription Initiation SiteOxidoreductasesLuciferaseResearch ArticleEchinodermsTranscriptional ActivationImaging TechniquesNeurogenesisGreen Fluorescent ProteinsEmbryonic DevelopmentSettore BIO/11 - Biologia MolecolareBiologyResearch and Analysis MethodsGenome ComplexityParacentrotus lividus03 medical and health sciencesSpecies SpecificityTubulinsbiology.animalFluorescence ImagingGeneticsmedicineConsensus sequenceAnimalsCiliaEnhancerBiochemistry Genetics and Molecular Biology (all)Binding SitesModels Geneticlcsh:REmbryosOrganismsBiology and Life SciencesComputational BiologyProteinsbiology.organism_classificationInvertebratesIntronsCytoskeletal Proteins030104 developmental biologyAgricultural and Biological Sciences (all)Bright Field ImagingSea UrchinsEnzymologyMutagenesis Site-Directedlcsh:QTransmission Electron MicroscopyDevelopmental BiologyTranscription FactorsPLOS ONE
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Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer.

2016

Abstract As a master regulator of chromatin function, the lysine methyltransferase EZH2 orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non–small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 remains elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with new genetically engineered mouse models of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways, leading to epigenetic transformation independent of canonical growth factor pathway activation. As such, tumors feature a transcrip…

0301 basic medicineModels MolecularLung Neoplasmsmedicine.medical_treatmentMolecular ConformationGene ExpressionAntineoplastic Agentsmacromolecular substancesBiologymedicine.disease_causeArticleMalignant transformationTargeted therapy03 medical and health sciencesMiceStructure-Activity RelationshipCell Line TumormedicineAnimalsHumansEnhancer of Zeste Homolog 2 ProteinMolecular Targeted TherapyLung cancerPromoter Regions GeneticGene Expression ProfilingEZH2Cancermedicine.diseaseMagnetic Resonance ImagingXenograft Model Antitumor AssaysChromatinrespiratory tract diseasesGene Expression Regulation NeoplasticDisease Models Animal030104 developmental biologyCell Transformation NeoplasticEnhancer Elements GeneticOncologyDrug DesignCancer researchAdenocarcinomaKRASEpigenetic therapyCancer discovery
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Transcriptomic data from panarthropods shed new light on the evolution of insulator binding proteins in insects : Insect insulator proteins.

2016

Background Body plan development in multi-cellular organisms is largely determined by homeotic genes. Expression of homeotic genes, in turn, is partially regulated by insulator binding proteins (IBPs). While only a few enhancer blocking IBPs have been identified in vertebrates, the common fruit fly Drosophila melanogaster harbors at least twelve different enhancer blocking IBPs. We screened recently compiled insect transcriptomes from the 1KITE project and genomic and transcriptomic data from public databases, aiming to trace the origin of IBPs in insects and other arthropods. Results Our study shows that the last common ancestor of insects (Hexapoda) already possessed a substantial number …

0301 basic medicineMost recent common ancestormedia_common.quotation_subjectInsectDipluraGene evolutionEvolution Molecular03 medical and health sciencesArthropod evolutionGeneticsAnimalsEnhancerArthropodsPhylogenymedia_commonGeneticsbiologyGene Expression ProfilingfungiComparative transcriptomic analysesbiology.organism_classificationInsulator binding proteinsNeopteraDNA-Binding Proteins030104 developmental biologyBody planDrosophila melanogasterEnhancer Elements GeneticInsulator ElementsDrosophila melanogasterHomeotic geneTranscriptomeBiotechnologyResearch ArticleBMC genomics
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Epigenomic landscape of human colorectal cancer unveils an aberrant core of pan-cancer enhancers orchestrated by YAP/TAZ

2021

Cancer is characterized by pervasive epigenetic alterations with enhancer dysfunction orchestrating the aberrant cancer transcriptional programs and transcriptional dependencies. Here, we epigenetically characterize human colorectal cancer (CRC) using de novo chromatin state discovery on a library of different patient-derived organoids. By exploring this resource, we unveil a tumor-specific deregulated enhancerome that is cancer cell-intrinsic and independent of interpatient heterogeneity. We show that the transcriptional coactivators YAP/TAZ act as key regulators of the conserved CRC gained enhancers. The same YAP/TAZ-bound enhancers display active chromatin profiles across diverse human t…

0301 basic medicineOrganoidEpigenomicsTranscription FactorGeneral Physics and AstronomyColorectal NeoplasmAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Tumor Cells Cultured; Enhancer Elements Genetic; Epigenesis GeneticEpigenesis Genetic0302 clinical medicineModelsAdaptor Proteins Signal Transducing Colorectal Neoplasms Gene Expression Regulation NeoplasticHistone Code Humans Models Genetic Organoids RNA-Seq Single-Cell Analysis Trans-Activators Transcription Factors Tumor Cells Cultured Enhancer Elements Genetic Epigenesis GeneticTumor Cells CulturedCancer genomicsHistone codeRNA-SeqEpigenomicsAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Transcriptional Coactivator with PDZ-Binding Motif Proteins; Tumor Cells Cultured; YAP-Signaling Proteins; Enhancer Elements Genetic; Epigenesis GeneticMultidisciplinaryCulturedQAdaptor Proteins3. Good healthChromatinTumor CellsGene Expression Regulation NeoplasticHistone CodeOrganoidsSingle-Cell AnalysiEnhancer Elements GeneticTrans-Activator030220 oncology & carcinogenesisSingle-Cell AnalysisColorectal NeoplasmsHumanEnhancer ElementsScienceTumour heterogeneityBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesGeneticmedicineHumansEpigeneticsEnhancerTranscription factorAdaptor Proteins Signal TransducingNeoplasticModels GeneticSignal TransducingCancerYAP-Signaling ProteinsGeneral Chemistrymedicine.diseaseColorectal cancerdigestive system diseases030104 developmental biologyGene Expression RegulationTranscriptional Coactivator with PDZ-Binding Motif ProteinsCancer cellCancer researchTrans-ActivatorsEpigenesisTranscription Factors
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Co-regulation of paralog genes in the three-dimensional chromatin architecture.

2016

Paralog genes arise from gene duplication events during evolution, which often lead to similar proteins that cooperate in common pathways and in protein complexes. Consequently, paralogs show correlation in gene expression whereby the mechanisms of co-regulation remain unclear. In eukaryotes, genes are regulated in part by distal enhancer elements through looping interactions with gene promoters. These looping interactions can be measured by genome-wide chromatin conformation capture (Hi-C) experiments, which revealed self-interacting regions called topologically associating domains (TADs). We hypothesize that paralogs share common regulatory mechanisms to enable coordinated expression acco…

0301 basic medicineanimal structuresComputational biologyBiologyGenomeChromosome conformation capture03 medical and health sciencesMice0302 clinical medicineDogsGene DuplicationGene duplicationGeneticsAnimalsCluster AnalysisHumansPromoter Regions GeneticGeneChIA-PETGenomic organizationGeneticsRegulation of gene expressionGenomefungiGene regulation Chromatin and EpigeneticsComputational BiologyChromatin Assembly and DisassemblyBiological EvolutionChromatinChromatin030104 developmental biologyEnhancer Elements GeneticGene Expression Regulation030217 neurology & neurosurgeryNucleic acids research
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Association Between ABCB1 Genetic Variants and Persistent Chemotherapy-Induced Alopecia in Women With Breast Cancer

2020

Importance Persistent chemotherapy-induced alopecia (pCIA) has been recently described in patients with breast cancer and in its most severe form occurs in up to 10% of these patients. Genetic risk factors associated with pCIA have not been adequately explored. Objective To identify genetic variants associated with pCIA. Design, Setting, and Participants In this genetic association study, 215 women with breast cancer treated with docetaxel-based chemotherapy with a follow-up of 1.5 to 10 years after the end of the treatment were recruited retrospectively through 3 hospital oncology units across Spain between 2005 and 2018. Severe pCIA was defined as lack of scalp hair recovery (Common Termi…

AdultOncologymedicine.medical_specialtyATP Binding Cassette Transporter Subfamily BBiopsyBreast NeoplasmsGenome-wide association studyDocetaxelDermatologyPolymorphism Single Nucleotide030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineBreast cancerRisk FactorsInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansGenetic Predisposition to DiseasePromoter Regions GeneticAdverse effectRetrospective StudiesDose-Response Relationship Drugbusiness.industryAge FactorsCase-control studyAlopeciaCommon Terminology Criteria for Adverse EventsRetrospective cohort studyOdds ratioMiddle Agedmedicine.diseaseEnhancer Elements GeneticDocetaxelCase-Control Studies030220 oncology & carcinogenesisFemalebusinessHair FollicleFollow-Up StudiesGenome-Wide Association Studymedicine.drugJAMA Dermatology
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Negative Regulation of β Enolase Gene Transcription in Embryonic Muscle Is Dependent upon a Zinc Finger Factor That Binds to the G-rich Box within th…

1998

We have previously identified a muscle-specific enhancer within the first intron of the human beta enolase gene. Present in this enhancer are an A/T-rich box that binds MEF-2 protein(s) and a G-rich box (AGTGGGGGAGGGGGCTGCG) that interacts with ubiquitously expressed factors. Both elements are required for tissue-specific expression of the gene in skeletal muscle cells. Here, we report the identification and characterization of a Kruppel-like zinc finger protein, termed beta enolase repressor factor 1, that binds in a sequence-specific manner to the G-rich box and functions as a repressor of the beta enolase gene transcription in transient transfection assays. Using fusion polypeptides of b…

AgingTranscription GeneticMolecular Sequence DataDown-RegulationRepressorRegulatory Sequences Nucleic AcidBiologyBiochemistryDNA-binding proteinGene Expression Regulation EnzymologicMiceGene expressionAnimalsHumansAmino Acid SequenceCloning MolecularMuscle SkeletalEnhancerMolecular BiologyCell NucleusRegulation of gene expressionZinc fingerSp1 transcription factorBinding SitesSequence Homology Amino AcidZinc FingersCell BiologyMolecular biologyDNA-Binding ProteinsEnhancer Elements GeneticRegulatory sequencePhosphopyruvate HydrataseJournal of Biological Chemistry
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Enhancer trap infidelity in Drosophila optomotor-blind

2013

Reporter gene activity in enhancer trap lines is often implicitly assumed to mirror quite faithfully the endogenous expression of the "trapped" gene, even though there are numerous examples of enhancer trap infidelity. optomotor-blind (omb) is a 160 kb gene in which 16 independent P-element enhancer trap insertions of three different types have been mapped in a range of more than 60 kb. We have determined the expression pattern of these elements in wing, eye-antennal and leg imaginal discs as well as in the pupal tergites. We noted that one pGawB insertion (omb (P4) ) selectively failed to report parts of the omb pattern even though the missing pattern elements were apparent in all other 15…

Arthropod AntennaeNerve Tissue ProteinsEyeGenes ReporterEnhancer trapAnimalsDrosophila ProteinsWings AnimalDrosophila (subgenus)EnhancerPromoter Regions GeneticGeneGeneticsReporter genebiologyPupaChromosome MappingPromoterExtremitiesbiology.organism_classificationImaginal discMutagenesis InsertionalEnhancer Elements GeneticImaginal DiscsInsect ScienceDrosophilaT-Box Domain ProteinsDrosophila ProteinResearch Paper
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