Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE21953
PROVIDER: PRJNA127243 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-wide binding pattern of PU.1 in normal erythroid progenitors and erythroleukemia cells
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Project description:Transcriptome analysis of normal erythroid progenitors and erythroleukemia cells
| PRJNA129389 | ENA
Project description:We find that the myeloid master regulatory transcription factor, PU.1, binds to >16,000 sites in both normal and leukemic erythroid cells. Of these bound sites, ~7,000 lie within 2kb of TSS of a gene, suggesting PU.1 may regulate a large number of genes in erythroid cells. Coupling this data with gene expression analysis, we show PU.1 directly regulates several critical signaling pathways in erythroid cells. Assaying PU.1 occupancy in normal and leukemic erythroid cells
2011-06-23 | E-GEOD-21950 | biostudies-arrayexpress
Project description:We find that the myeloid master regulatory transcription factor, PU.1, binds to >16,000 sites in both normal and leukemic erythroid cells. Of these bound sites, ~7,000 lie within 2kb of TSS of a gene, suggesting PU.1 may regulate a large number of genes in erythroid cells. Coupling this data with gene expression analysis, we show PU.1 directly regulates several critical signaling pathways in erythroid cells.
2011-06-23 | GSE21950 | GEO
Project description:To promote the development and understanding of the in vitro erythroleukemia model, we analyzed the transcriptomes of mouse erythroleukemia (MEL) cells prior to and after erythroid-like differentiation induced by dimethyl sulfoxide (DMSO). A total of 348 protein-coding genes, including many known erythroid-enriched genes such as hemoglobin and heme synthesis genes, were upregulated upon erythroid-like induction in MEL cells
2019-10-01 | GSE133343 | GEO
Project description:We find GATA-1 occupies 6,600 sites in proliferating erythroid progenitors and 10,600 sites in differentiating progenitors. 80-90% of GATA-1 binds within intragenic or intergenic regions, while <20% of GATA-1 is found within 2kb of TSS. Assaying GATA-1 occupancy in normal erythroid progenitors in both proliferating and differentiating conditions.
2012-02-27 | E-GEOD-35379 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE35379: Genome-wide occupancy map of GATA-1 in proliferating and differentiating murine ES cell derived erythroid progenitors (ES-EP) GSE35384: Transcriptome analysis of differentiating normal and leukemic erythroid progenitors Refer to individual Series
2012-02-27 | E-GEOD-35385 | biostudies-arrayexpress
Project description:Oncogenic mutations confer aberrant replicative capacity to cells with little or no replicative capacity, generating cancer stem cells that perpetuate the tumor through extensive self-replication and differentiation blockade. However, whether oncogenes disrupt the cellular identity of cancer stem cell by altering the developmental potential is unknown. Fate conversion has been demonstrated by ectopic expression of master transcriptional regulators, such as PU.1 and C/EBPα that confers myeloid cell fate to other cell types, and PRDM16 that confers brown adipose fate to white adipocytes or myoblasts. Here we show that a transcriptional regulator overexpressed in human myeloid malignancies, PRDM16s, causes oncogenic fate conversion, by transforming cells fated to form platelets and erythrocytes into myeloid leukemia-initiating cells (LICs). Prdm16s expression in murine hematopoietic progenitor cells caused a myelodysplastic syndrome (MDS)-like disease that progressed to acute myelogenous leukemia (AML). The myeloid diseases caused by Prdm16s exhibited expansion of megakaryocyte-erythroid progenitors (MEPs) but not granulocyte-macrophage progenitors. MEPs from Prdm16s-induced leukemia possessed LIC potential, and expression of Prdm16s in normal MEPs was sufficient to convert them to myeloid LICs and blocked megakaryocytic/erythroid potential. Prdm16s induced the expression of myeloid master regulators, including PU.1 and C/EBPα, by interacting with their super enhancers. Ablation of myeloid master regulators attenuated the myeloid potential and reinstalled the megakaryocytic/erythroid potential of leukemic-MEPs in mouse models and in human AML with PRDM16 rearrangement. Our study demonstrates that oncogenic PRDM16 expression converts the fate of MEPs to a malignant myeloid fate by activating myeloid master transcription factors.
2019-03-01 | GSE119301 | GEO
Project description:Oncogenic mutations confer aberrant replicative capacity to cells with little or no replicative capacity, generating cancer stem cells that perpetuate the tumor through extensive self-replication and differentiation blockade. However, whether oncogenes disrupt the cellular identity of cancer stem cell by altering the developmental potential is unknown. Fate conversion has been demonstrated by ectopic expression of master transcriptional regulators, such as PU.1 and C/EBPα that confers myeloid cell fate to other cell types, and PRDM16 that confers brown adipose fate to white adipocytes or myoblasts. Here we show that a transcriptional regulator overexpressed in human myeloid malignancies, PRDM16s, causes oncogenic fate conversion, by transforming cells fated to form platelets and erythrocytes into myeloid leukemia-initiating cells (LICs). Prdm16s expression in murine hematopoietic progenitor cells caused a myelodysplastic syndrome (MDS)-like disease that progressed to acute myelogenous leukemia (AML). The myeloid diseases caused by Prdm16s exhibited expansion of megakaryocyte-erythroid progenitors (MEPs) but not granulocyte-macrophage progenitors. MEPs from Prdm16s-induced leukemia possessed LIC potential, and expression of Prdm16s in normal MEPs was sufficient to convert them to myeloid LICs and blocked megakaryocytic/erythroid potential. Prdm16s induced the expression of myeloid master regulators, including PU.1 and C/EBPα, by interacting with their super enhancers. Ablation of myeloid master regulators attenuated the myeloid potential and reinstalled the megakaryocytic/erythroid potential of leukemic-MEPs in mouse models and in human AML with PRDM16 rearrangement. Our study demonstrates that oncogenic PRDM16 expression converts the fate of MEPs to a malignant myeloid fate by activating myeloid master transcription factors.
2019-03-01 | GSE119300 | GEO
Project description:Transcriptome analysis of differentiating normal and leukemic erythroid progenitors
| PRJNA156067 | ENA