Search results for "Enhancer"

showing 10 items of 148 documents

Computational processing and quality control of Hi-C, capture Hi-C and capture-C data

2019

Hi-C, capture Hi-C (CHC) and Capture-C have contributed greatly to our present understanding of the three-dimensional organization of genomes in the context of transcriptional regulation by characterizing the roles of topological associated domains, enhancer promoter loops and other three-dimensional genomic interactions. The analysis is based on counts of chimeric read pairs that map to interacting regions of the genome. However, the processing and quality control presents a number of unique challenges. We review here the experimental and computational foundations and explain how the characteristics of restriction digests, sonication fragments and read pairs can be exploited to distinguish…

0301 basic medicine570lcsh:QH426-470media_common.quotation_subjectContext (language use)ReviewComputational biologyBiologyProcessingGenome576Capture Hi-C03 medical and health sciences0302 clinical medicineHi-CDatabases GeneticGeneticsTranscriptional regulationHumansQuality (business)EnhancerControl (linguistics)Genetics (clinical)media_commonGenomeChromosome MappingComputational BiologyHigh-Throughput Nucleotide SequencingQuality controlGenomicsChromatin004Chromatinlcsh:Genetics030104 developmental biology030220 oncology & carcinogenesis
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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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Haploinsufficiency of the Primary Familial Brain Calcification Gene SLC20A2 Mediated by Disruption of a Regulatory Element

2020

OBJECTIVE Primary familial brain calcification (PFBC) is a rare cerebral microvascular calcifying disorder with diverse neuropsychiatric expression. Five genes were reported as PFBC causative when carrying pathogenic variants. Haploinsufficiency of SLC20A2, which encodes an inorganic phosphate importer, is a major cause of autosomal-dominant PFBC. However, PFBC remains genetically unexplained in a proportion of patients, suggesting the existence of additional genes or cryptic mutations. We analyzed exome sequencing data of 71 unrelated, genetically unexplained PFBC patients with the aim to detect copy number variations that may disrupt the expression of core PFBC-causing genes. METHODS Afte…

0301 basic medicineBrain DiseasesDNA Copy Number VariationsSodium-Phosphate Cotransporter Proteins Type IIIHEK 293 cellsBrainHaploinsufficiencyBiologyMolecular biologyReverse transcriptase03 medical and health sciencesHEK293 Cells030104 developmental biology0302 clinical medicineNeurologyMutationHumansNeurology (clinical)Copy-number variationAlleleHaploinsufficiencyEnhancerGene030217 neurology & neurosurgeryExome sequencingMovement Disorders
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Epigenetic Silencing of CDR1as Drives IGF2BP3-Mediated Melanoma Invasion and Metastasis.

2018

Summary Metastasis is the primary cause of death of cancer patients. Dissecting mechanisms governing metastatic spread may uncover important tumor biology and/or yield promising therapeutic insights. Here, we investigated the role of circular RNAs (circRNA) in metastasis, using melanoma as a model aggressive tumor. We identified silencing of cerebellar degeneration-related 1 antisense (CDR1as), a regulator of miR-7, as a hallmark of melanoma progression. CDR1as depletion results from epigenetic silencing of LINC00632, its originating long non-coding RNA (lncRNA) and promotes invasion in vitro and metastasis in vivo through a miR-7-independent, IGF2BP3-mediated mechanism. Moreover, CDR1as le…

0301 basic medicineCancer ResearchRegulatorNerve Tissue ProteinsBiologyAutoantigensArticleMetastasisEpigenesis Genetic03 medical and health sciences0302 clinical medicinemedicineGene silencingHumansEnhancer of Zeste Homolog 2 ProteinNeoplasm InvasivenessRNA AntisenseGene SilencingNeoplasm MetastasisMelanomaMelanomaEZH2RNACancerRNA-Binding ProteinsRNA Circularmedicine.diseasePhospholipid Hydroperoxide Glutathione PeroxidasePrognosisMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchbiology.proteinRNA Long NoncodingPRC2Cancer cell
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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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Epigenetic Regulation of Cardiac Differentiation of Embryonic Stem Cells and Tissues.

2016

International audience; Specific gene transcription is a key biological process that underlies cell fate decision during embryonic development. The biological process is mediated by transcription factors which bind genomic regulatory regions including enhancers and promoters of cardiac constitutive genes. DNA is wrapped around histones that are subjected to chemical modifications. Modifications of histones further lead to repressed, activated or poised gene transcription, thus bringing another level of fine tuning regulation of gene transcription. Embryonic Stem cells (ES cells) recapitulate within embryoid bodies (i.e., cell aggregates) or in 2D culture the early steps of cardiac developme…

0301 basic medicineCellular differentiationGeneral Chemical Engineering[SDV]Life Sciences [q-bio]Human Embryonic Stem Cellscardiac developmentcardiac differentiationEmbryoid bodychromatin immunoprecipitationBiologyGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticHistones03 medical and health sciencesMiceIssue 112AnimalsHumansEpigeneticsEnhancerTranscription factorGeneticsGeneral Immunology and MicrobiologyGeneral NeurosciencePromoterCell DifferentiationHeartgene transcription regulationEmbryonic stem cellES cellsCell biology[SDV] Life Sciences [q-bio]030104 developmental biologyEpigeneticsChromatin immunoprecipitationDevelopmental Biology
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CRISPR-Cas9 screen reveals a MYCN-amplified neuroblastoma dependency on EZH2.

2018

Pharmacologically difficult targets, such as MYC transcription factors, represent a major challenge in cancer therapy. For the childhood cancer neuroblastoma, amplification of the oncogene MYCN is associated with high-risk disease and poor prognosis. Here, we deployed genome-scale CRISPR-Cas9 screening of MYCN-amplified neuroblastoma and found a preferential dependency on genes encoding the polycomb repressive complex 2 (PRC2) components EZH2, EED, and SUZ12. Genetic and pharmacological suppression of EZH2 inhibited neuroblastoma growth in vitro and in vivo. Moreover, compared with neuroblastomas without MYCN amplification, MYCN-amplified neuroblastomas expressed higher levels of EZH2. ChIP…

0301 basic medicineCellular differentiationMedical and Health SciencesNeuroblastomaSUZ12Oncogene MYCNCRISPR-Cas SystemCancerPediatricNeuronsN-Myc Proto-Oncogene ProteinTumorEZH2EpigeneticCell DifferentiationGeneral MedicineUp-RegulationGene Expression Regulation NeoplasticOncology5.1 PharmaceuticalsEpigeneticsDevelopment of treatments and therapeutic interventionsHumanResearch ArticlePediatric Research InitiativePediatric CancerImmunologymacromolecular substancesBiologyN-Myc Proto-Oncogene ProteinCell Line03 medical and health sciencesRare DiseasesNeuroblastomaCell Line TumormedicineGeneticsHumansEnhancer of Zeste Homolog 2 ProteinTranscription factorneoplasmsNeoplasticHuman GenomeNeurosciencesGene AmplificationNeuronmedicine.disease030104 developmental biologyGene Expression RegulationCancer researchHistone deacetylaseCRISPR-Cas SystemsThe Journal of clinical investigation
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Contribution of allelic imbalance to colorectal cancer

2018

Point mutations in cancer have been extensively studied but chromosomal gains and losses have been more challenging to interpret due to their unspecific nature. Here we examine high-resolution allelic imbalance (AI) landscape in 1699 colorectal cancers, 256 of which have been whole-genome sequenced (WGSed). The imbalances pinpoint 38 genes as plausible AI targets based on previous knowledge. Unbiased CRISPR-Cas9 knockout and activation screens identified in total 79 genes within AI peaks regulating cell growth. Genetic and functional data implicate loss of TP53 as a sufficient driver of AI. The WGS highlights an influence of copy number aberrations on the rate of detected somatic point muta…

0301 basic medicineDenmarkLoss of HeterozygosityGeneral Physics and AstronomyAllelic ImbalanceLoss of heterozygosityGenotypeddc:576.5RNA Small Interferinglcsh:ScienceRNA Small Interfering/geneticsGeneticsMultidisciplinaryQGenomicsPhenotype3. Good healthGENOMEPhenotypesyöpägeenitAllelic ImbalanceTumor Suppressor Protein p53/geneticsColorectal NeoplasmsChromosomes Human Pair 8GENESDNA Copy Number VariationsGenotypeScienceTranscription Factors/geneticsGenomicscolorectal cancerBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins p21(ras)Proto-Oncogene Proteins p21(ras)/genetics03 medical and health sciencesmedicineHumansPoint MutationGenetic Predisposition to DiseaseGenepaksusuolisyöpäChromosome AberrationsWhole Genome SequencingHUMAN-COLONGene Expression ProfilingPoint mutationCancerGeneral Chemistrymedicine.diseaseColorectal Neoplasms/geneticsENHANCERS030104 developmental biologyCELLSlcsh:Q3111 BiomedicineTumor Suppressor Protein p53CRISPR-Cas SystemsmutaatiotTranscription FactorsMicrosatellite Repeats
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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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The Sea Urchin sns5 Chromatin Insulator Shapes the Chromatin Architecture of a Lentivirus Vector Integrated in the Mammalian Genome.

2016

Lentivirus vectors are presently the favorite vehicles for therapeutic gene transfer in hematopoietic cells. Nonetheless, these vectors integrate randomly throughout the genome, exhibiting variegation of transgene expression due to the spreading of heterochromatin into the vector sequences. Moreover, the cis-regulatory elements harbored by the vector could disturb the proper transcription of resident genes neighboring the integration site. The incorporation of chromatin insulators in flanking position to the transferred unit can alleviate both the above-mentioned dangerous effects, due to the insulator-specific barrier and enhancer-blocking activities. In this study, we report the valuable …

0301 basic medicineHeterochromatinTransgeneGenetic VectorsGreen Fluorescent ProteinsPharmaceutical ScienceGene ExpressionSettore BIO/11 - Biologia MolecolareBiochemistryGenomelentiviru03 medical and health sciencesMiceGeneticTranscription (biology)Genes ReporterTransduction GeneticCell Line TumorDrug DiscoveryGeneticsLeukocytesAnimalsHumansGATA1 Transcription FactorTransgenesEnhancerMolecular BiologyGenechromatin structureGeneticsGenomechromatin insulatorbiologyLentivirusbiology.organism_classificationgene therapyChromatinChromatinCell biology030104 developmental biologyHEK293 CellsSea UrchinsLentivirusMolecular MedicineBiological AssayInsulator Elementstransgene expressionHeLa CellsNucleic acid therapeutics
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