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ATAC-seq profiling of ER-Hoxa9-Lys-GFP cells before and after inducing irreversible commitment to myeloid differentiation

ABSTRACT: ATAC-seq profiling of ER-Hoxa9-Lys-GFP cells before and after inducing irreversible commitment to myeloid differentiation

PROVIDER: PRJNA738862 | ENA |

REPOSITORIES: ENA

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RNA-seq profiling of ER-Hoxa9-Lys-GFP cells before and after inducing irreversible commitment to myeloid differentiation

Project description:RNA-seq profiling of ER-Hoxa9-Lys-GFP cells before and after inducing irreversible commitment to myeloid differentiation

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ATAC-seq profiling of ER-Hoxa9-Lys-GFP cells before and after inducing irreversible commitment to myeloid differentiation

Project description:Data reveal epigenome-wide trends associated with irreversible commitment from the GMP-like state to the neutrophil-like state

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RNA-seq profiling of ER-Hoxa9-Lys-GFP cells before and after inducing irreversible commitment to myeloid differentiation

Project description:Data reveal transcriptome-wide gene expression trends associated with irreversible commitment from the GMP-like state to the neutrophil-like state

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ChIP-seq profiling of H3K4me3, H3K27ac, H3K27me3, V5-HOXA9-AM, and V5-ER-HOXA9-AM cells before and after inducing irreversible commitment to myeloid differentiation

Project description:Data reveal epigenome-wide trends in histone modifications and Hoxa9 binding sites associated with irreversible commitment from the GMP-like state to the neutrophil-like state

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ChIP-seq profiling of H3K4me3, H3K27ac, H3K27me3, V5-HOXA9-AM, and V5-ER-HOXA9-AM cells before and after inducing irreversible commitment to myeloid differentiation

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ATAC-seq profiling of ER-Hoxa9-Lys-GFP cells over myeloid differentiation program

Project description:ATAC-seq profiling of ER-Hoxa9-Lys-GFP cells over myeloid differentiation program

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Reduced representation bisulfite sequencing (RRBS) profiling of ER-Hoxa9-Lys-GFP cells over myeloid differentiation program

Project description:Reduced representation bisulfite sequencing (RRBS) profiling of ER-Hoxa9-Lys-GFP cells over myeloid differentiation program

| PRJNA761198 | ENA

MicroRNA-155 is upregulated in Hoxa9/Meis1 leukemia inducing cells but is dispensable for in vivo transformation and leukemia development

Project description:OBJECTIVE: The microRNA miR-155 is upregulated in Hoxa9 and Meis1 leukemia inducing cells (LIC) , and miR-155 accelerates the onset of acute myeloid leukemia (AML) together with Hoxa9 but through largely unknown molecular mechanisms. The impact of miR-155 on accelerated onset of leukemia in the context of Hoxa9 and Meis1 is also unclear. To further resolve this, we performed a gene expression profiling, in the context of Hoxa9 and Meis1 leukemogenesis with miR-155 knocked out. RESULTS: Gene expression profiling of Hoxa9/Meis1 LIC without miR-155 does not delay the onset of AML and the gene expression changes are small

2017-04-27 | GSE80660 | GEO

The Growth factor independence 1 (GFI1) 36N variant predisposes to Acute Myeloid Leukemia (AML) by inducing epigenetic changes at the Hoxa9 locus

Project description:GFI136N is a coding Single Nucleotide Polymorphism (SNP) in the gene GFI1 that increases the risk for Acute myeloid leukemia (AML) by 60%. It is present in 3-5% of Caucasians and has a prevalence of 12% among AML patients. We generated knockin mice expressing either the human GFI136N variant or the more common GFI136S form and observed that GFI136N, in contrast to GFI136S, lacked the ability to bind to the Gfi1 target gene and leukemia associated transcription factor Hoxa9 in myeloid precursors and failed to initiate the histone modifications that regulate HoxA9 expression. Consistent with this, GFI136N heterozygous AML patients showed increased HOXA9 expression compared to control patients. In the knockin mice, granulo-monocytic pogenitors (GMPs), a bone marrow subset from which AML can arise, show a proliferative expansion in the presence of the GFI136N variant. Finally, the GFI136N variant increased colony formation and proliferation of myeloid precursors induced by the onco-fusion proteins MLL/AF9 or AML1/Eto9a and accelerated the onset of a KRAS-driven myelo-proliferative disease. Our data suggest that GFI136N predisposes to AML by deregulating the expression of Hoxa9, a locus highly relevant for AML, thereby inducing a pre-leukemic state in myeloid precursors that can give rise to AML. 3 samples (2 histone modifications, 1 transcription factor)

2012-12-04 | E-GEOD-31657 | biostudies-arrayexpress

Time course of myeloid differentiation in the Lysozyme-GFP ER-HoxA9 cells following estradiol withdrawal

Project description:Lysozyme-GFP ER-HoxA9 cells were cultured in the presence of estradiol (active ER-HoxA9) or in the absence of estradiol (inactive ER-HoxA9). Samples were taken at 10 time points over a 120 hour time course of myeloid differentiation to examine those gene expression changes that accompany differentiation upon the release of HoxA9 differentiation arrest.

2016-10-01 | GSE84874 | GEO

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