Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA184065 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Effect of lentiviral-based shRNA-mediated knockdown of ZFX on the human medulloblastoma (MB) cell-line DAOY
| PRJNA193340 | ENA
Project description:shRNA mediated knockdown of TRA2B and SRSF3 in HEK293 cell line
| PRJNA151827 | ENA
Project description:Acute myeloid leukemia (AML) and acute T-lymphoblastic leukemia (T-ALL) maintain the undifferentiated phenotype and proliferative capacity of their respective cells of origin, hematopoietic stem/progenitor cells and immature thymocytes. The mechanisms that maintain these progenitor-like characteristics are poorly understood. We report that the transcription factor Zfx is required for the development and propagation of experimental AML caused by MLL-AF9 fusion, and of T-ALL caused by Notch1 activation. In both leukemia types, Zfx activated progenitor-associated gene expression programs and prevented differentiation. Key Zfx target genes included mitochondrial enzymes Ptpmt1 and Idh2, whose overexpression partially rescued the propagation of Zfx-deficient AML. These studies identify a common mechanism that controls the cell-of-origin characteristics of acute leukemias derived from disparate lineages and transformation mechanisms. NOMO-1 cells were infected with control and ZFX shRNA lentiviruses at an MOI of 1. RNA was collected for microarrays 48 hours after selection.
2015-01-01 | E-GEOD-43021 | biostudies-arrayexpress
Project description:Acute myeloid leukemia (AML) and acute T-lymphoblastic leukemia (T-ALL) maintain the undifferentiated phenotype and proliferative capacity of their respective cells of origin, hematopoietic stem/progenitor cells and immature thymocytes. The mechanisms that maintain these progenitor-like characteristics are poorly understood. We report that transcription factor Zfx is required for the development and propagation of experimental AML caused by MLL-AF9 fusion, and of T-ALL caused by Notch1 activation. In both leukemia types, Zfx activated progenitor-associated gene expression programs and prevented differentiation. Key Zfx target genes included mitochondrial enzymes Ptpmt1 and Idh2, whose overexpression partially rescued the propagation of Zfx-deficient AML. These studies identify a common mechanism that controls the cell-of-origin characteristics of acute leukemias derived from disparate lineages and transformation mechanisms. Analysis of genomic ZFX binding in the AML cell line NOMO-1 and the T-ALL cell line RPMI-8402
2014-01-30 | E-GEOD-43147 | biostudies-arrayexpress
Project description:Effect of HOXA9 shRNA versus DB1055 treatment of human THP-1 AML cell line
2020-11-13 | GSE106831 | GEO
Project description:Anti-ZFX ChIP-seq in a human medulloblastoma cell line
| PRJNA194396 | ENA
Project description:Gene expression profiles induced by shRNA-mediated knockdown of PDEF in MCF7 mammary epithelial cell line
| PRJNA175497 | ENA
Project description:shRNA knockdown of ZMIZ1 in human T-cell Acute Lymphoblastic Leukemia cell line CEM
| PRJNA147833 | ENA
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO