0000000000423183

AUTHOR

Nina Cabezas-wallscheid

showing 3 related works from this author

In vivo fate mapping with SCL regulatory elements identifies progenitors for primitive and definitive hematopoiesis in mice.

2009

10 páginas, 6 figuras.-- et al.

Definitive hematopoiesisEmbryologyMyeloidPopulationConditional mouse modelIn vivo linage and fate tracingEmbryonic DevelopmentStem cell leukemia geneBiology03 medical and health sciencesMice0302 clinical medicineFate mappinghemic and lymphatic diseasesProto-Oncogene ProteinsCRE systemmedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsCell LineageMesodermal blood cell specificationGene Knock-In TechniquesProgenitor celleducationGeneTetracycline systemT-Cell Acute Lymphocytic Leukemia Protein 1Primitive hematopoiesis030304 developmental biology0303 health scienceseducation.field_of_studyMicroscopy ConfocalStem CellsEmbryoFlow CytometryCell biologyHematopoiesisGastrulationHaematopoiesismedicine.anatomical_structureBlood cell precursors030220 oncology & carcinogenesisImmunologyIn vivo lineage markingDevelopmental BiologyMechanisms of development
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Instruction of haematopoietic lineage choices, evolution of transcriptional landscapes and cancer stem cell hierarchies derived from an AML1-ETO mous…

2013

The t(8;21) chromosomal translocation activates aberrant expression of the AML1-ETO (AE) fusion protein and is commonly associated with core binding factor acute myeloid leukaemia (CBF AML). Combining a conditional mouse model that closely resembles the slow evolution and the mosaic AE expression pattern of human t(8;21) CBF AML with global transcriptome sequencing, we find that disease progression was characterized by two principal pathogenic mechanisms. Initially, AE expression modified the lineage potential of haematopoietic stem cells (HSCs), resulting in the selective expansion of the myeloid compartment at the expense of normal erythro- and lymphopoiesis. This lineage skewing was foll…

cancer stem cellsCancer stem cells; Core binding factor acute myeloid leukaemia; Preclinical mouse model; Therapy target validation; Whole transcriptome sequencingMyeloidtherapy target validationOncogene Proteins FusionCloseupsBiologyGranulocyte-Macrophage Progenitor CellsTranslocation Geneticwhole transcriptome sequencingImmunophenotypingMiceGranulocyte-Macrophage Progenitor CellsCancer stem cellhemic and lymphatic diseasesmedicineAML1-ETOAnimalsCell Lineageacute myeloid leukaemiaLymphopoiesisProgenitor cellt(8;21)Research Articlespreclinical mouse modelGeneticsRegulation of gene expressionAntibiotics AntineoplasticSequence Analysis RNAcore binding factor acute myeloid leukaemiainducible mouse-modelHematopoietic Stem CellsMice Inbred C57BLDisease Models AnimalLeukemia Myeloid AcuteHaematopoiesisPhenotypemedicine.anatomical_structureGene Expression RegulationDoxorubicinCancer researchNeoplastic Stem CellsMolecular MedicineStem cell
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Generation and characterization of tTS-H4: a novel transcriptional repressor that is compatible with the reverse tetracycline-controlled TET-ON system

2007

Background Conditional gene regulatory systems ensuring tight and adjustable expression of therapeutic genes are central for developing future gene therapy strategies. Among various regulatory systems, tetracycline-controlled gene expression has emerged as a safe and reliable option. Moreover, the tightness of tetracycline-regulated gene switches can be substantially improved by complementing transcriptional activators with antagonizing repressors. Methods To develop novel tetracycline-responsive transcriptional repressors, we fused various transcriptional silencing domains to the TetR (B/E) DNA-binding and dimerization domain of the Tn10-encoded tetracycline resistance operon (TetR (B/E)).…

Transcription GeneticOperonRepressorBiologyHistone DeacetylasesHistonesMicechemistry.chemical_compoundGenes ReporterDrug DiscoveryGeneticsAnimalsHumansGene silencingTetRPromoter Regions GeneticMolecular BiologyGenetics (clinical)Regulation of gene expressionYY1Genetic TherapyTetracyclineMolecular biologyHDAC4Repressor ProteinsGene Expression RegulationchemistryGATAD2BNIH 3T3 CellsMolecular Medicine
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