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ABSTRACT: Identification and characterization of Hoxa9 binding sites in hematopoietic cells

PROVIDER: PRJNA148821 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR387747.fastq.gz	Fastqsanger.gz
	SRR387748.fastq.gz	Fastqsanger.gz
	SRR387749.fastq.gz	Fastqsanger.gz
	SRR387750.fastq.gz	Fastqsanger.gz
	SRR387751.fastq.gz	Fastqsanger.gz

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Project description:Identification and Characterization of Hoxa9 Binding Sites in Hematopoietic Cells

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Identification and characterization of Hoxa9 binding sites in hematopoietic cells

Project description:This SuperSeries is composed of the following subset Series: GSE21299: Expression data from murine cell line transduced with epitope tagged forms of Hoxa9 GSE33509: Identification and Characterization of Hoxa9 Binding Sites in Hematopoietic Cells GSE33517: Epigenetic profiling of histone H3K4me1, H3K4me3, H3K27me3, H3ac, H4ac, CBP and P300 using ChIP-chip Refer to individual Series

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Genome-wide co-occupancy of Hoxa9 and C/EBPα in Hoxa9/Meis1 transformed HSCs [ChIP-seq]

Project description:Identification of the genome-wide binding sites of Hoxa9 and C/EBPα in a murine myeloblastic cell line transformed by Hoxa9/Meis1. Over 50% of Hoxa9 binding sites are co-bound by C/EBPα, providing mechanistic insight into the requirement of C/EBPα for Hoxa9-mediated leukemogenesis. Additionally, genome-wide occupancy of H3K4 monomethylation and H3K27 trimethylation provide additional information on the functionality of Hoxa9/C/EBPα cobound loci. Examination of two transcription factor binding sites and two histone modifications in a transformed cell line.

2014-06-11 | E-GEOD-58361 | biostudies-arrayexpress

Genome-wide co-occupancy of Hoxa9 and C/EBPα in Hoxa9/Meis1 transformed HSCs [ChIP-seq]

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Identification of genome wide Hoxa9 binding sites in primary murine and human AML cells

Project description:Relative overexpression of HOXA9 is a key feature of aggressive AML (acute myeloid leukemia). Here we determined genome wide binding sites of Hoxa9 in primary murine cells transformed by Hoxa9 and in a human AML cell line. In addition global H3K4 monomethylation and H3K27acetylation levels were determined in cells transformed by an inducible Hoxa9-ER construct in Hoxa9-active conditions and 72h after Hoxa9 was inactivated.

2019-04-13 | E-MTAB-7108 | biostudies-arrayexpress

Identification and Characterization of Hoxa9 Binding Sites in Hematopoietic Cells

Project description:The clustered homeobox proteins play crucial roles in development, hematopoiesis and leukemia yet the targets they regulate and their mechanisms of action are poorly understood. Here, we identified the binding sites for Hoxa9 and the Hox cofactor Meis1 on a genome-wide level and profiled their associated epigenetic modifications and transcriptional targets. Hoxa9 and the Hox cofactor Meis1 co-bind at hundreds of highly evolutionarily-conserved sites, most of which are distant from transcription start sites. These sites show high levels of histone H3K4 monomethylation and CBP/P300 binding characteristic of enhancers. Furthermore, a subset of these sites shows enhancer activity in transient transfection assays. Many Hoxa9 and Meis1 binding sites are also bound by PU.1 and other lineage-restricted transcription factors previously implicated in establishment of myeloid enhancers. Conditional Hoxa9 activation is associated with CBP/P300 recruitment, histone acetylation and transcriptional activation of a network of proto-oncogenes including Erg, Flt3, Lmo2, Myb and Sox4. Collectively this work suggests that Hoxa9 regulates transcription by interacting with enhancers of genes important for hematopoiesis and leukemia. To identify the genome-wide binding sites for Hoxa9 and the Hox cofactor Meis1

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Gene expression changes after loss of Hoxa9 in transformed HSCs [HOXA9 RNA-seq]

Project description:Characterization of gene expression changes 72 hours after withdrawal of tamoxifen in murine hematopoietic progenitors transformed by Hoxa9-ER/Meis1 using RNAseq. In the presence of tamoxifen (4OHT), Hoxa9-ER localizes to the nucleus of cells allowing for transformation, while withdrawal of 4OHT (culture in EtOH) leads to loss of nuclear Hoxa9-ER. Loss of Hoxa9-ER leads to a decrease in cellular proliferation and differentiation along the myeloid lineage.

2014-06-11 | GSE58359 | GEO

Gene expression changes after loss of Hoxa9 in transformed HSCs [HOXA9 RNA-seq]

2014-06-11 | E-GEOD-58359 | biostudies-arrayexpress

Identification of genome wide Hoxa9 binding sites in primary murine and human AML cells

Project description:Identification of genome wide Hoxa9 binding sites in primary murine and human AML cells

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Project description:We used ChIP-seq to examine the genome-wide binding of Nup98-HoxA9 and Crm1 in ES cells. Our analysis revealed that Nup98-HoxA9 is highly and preferentially targeted to specific chromatin sites, particularly near Hox cluster regions where the export factor Crm1 is originally prebound. chromatin immunoprecipitation

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