Genome-wide mapping of GATA2 in human iPS
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ABSTRACT:
PROVIDER: PRJNA420972 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-wide mapping of GATA2 in human iPS
2019-07-25 | GSE107639 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE34902: Genome-wide Profiling of Progesterone Receptor and GATA2 Binding in the Mouse Uterus [Affymetrix] GSE34927: Genome-wide Profiling of Progesterone Receptor and GATA2 Binding in the Mouse Uterus [ChIP-Seq] Refer to individual Series
2012-09-06 | E-GEOD-40663 | biostudies-arrayexpress
Project description:The transcription factor GATA2 is required for the expansion and differentiation of hematopoietic stem cells. GATA2 is also expressed in mesenchymal cells and was implicated in the regulation of adipocyte differentiation. Here we investigated genome-wide binding of endogenous GATA2 in mesenchymal cell lines and investigated the transcriptional responses of GATA2 overexpression in primary mesenchymal stem cells.
2018-04-17 | GSE101592 | GEO
Project description:We report the application of MNase-seq (Kent, Adams et al. 2011) to construct genome-wide nucleosome maps from human cells. To date, genome-wide changes in chromatin structure that occur during development in human cells have not been investigated widely. We have constructed and compared genome-wide chromatin maps from undifferentiated human iPS cells and and iPS cells differentiated to neural progenitor cells (NPC).
2019-04-24 | GSE117870 | GEO
Project description:GATA2 is well recognized as a key transcription factor and regulator of cell type specificity and differentiation. Here, we carried out comparative chromatin immunoprecipitation with comprehensive sequencing (ChIP-seq) to determine genome-wide occupancy of GATA2 in endothelial cells and erythroids, and compared the occupancy to the respective gene expression profile in each cell type. Although GATA2 was commonly expressed in both cell types, different GATA2 bindings and distinct cell specific gene expressions were observed. By using the ChIP-seq with epigenetic histone modifications and chromatin conformation capture assays; we elucidated the mechanistic regulation of endothelial-specific GATA2 mediated endomucin gene expression, that was regulated by the endothelial-specific chromatin loop with a GATA2 associated distal enhancer and core promoter. Knockdown of endomucin markedly attenuated endothelial cell growth, migration and tube formation. Moreover, abrogation of GATA2 in endothelium demonstrated not only a reduction of endothelial specific markers, but also induction of mesenchymal transition promoting gene expression. Our findings provide new insights into the correlation of endothelial expressed GATA2 binding, epigenetic modification, and the determination of endothelial cell specificity. Total 4 samples were derived from duplicate or triplicate arrays in HMVEC or K562 cells. Then, HMVEC were transfected with si-RNA against GATA2 in biological duplicate. Overall, 6 samples were uploaded.
2011-06-13 | E-GEOD-28304 | biostudies-arrayexpress
Project description:GATA2 is well recognized as a key transcription factor and regulator of cell type specificity and differentiation. Here, we carried out comparative chromatin immunoprecipitation with comprehensive sequencing (ChIP-seq) to determine genome-wide occupancy of GATA2 in endothelial cells and erythroids, and compared the occupancy to the respective gene expression profile in each cell type. Although GATA2 was commonly expressed in both cell types, different GATA2 bindings and distinct cell specific gene expressions were observed. By using the ChIP-seq with epigenetic histone modifications and chromatin conformation capture assays; we elucidated the mechanistic regulation of endothelial-specific GATA2 mediated endomucin gene expression, that was regulated by the endothelial-specific chromatin loop with a GATA2 associated distal enhancer and core promoter. Knockdown of endomucin markedly attenuated endothelial cell growth, migration and tube formation. Moreover, abrogation of GATA2 in endothelium demonstrated not only a reduction of endothelial specific markers, but also induction of mesenchymal transition promoting gene expression. Our findings provide new insights into the correlation of endothelial expressed GATA2 binding, epigenetic modification, and the determination of endothelial cell specificity.
2011-06-13 | GSE28304 | GEO
Project description:Genome-wide mapping of fission yeast
| PRJNA375807 | ENA
Project description:Progesterone (P4) signaling through its nuclear transcription factor, the progesterone receptor (PR), is essential for normal uterine function. Although deregulation of PR mediated signaling is known to underscore uterine dysfunction and a number of endometrial pathologies, the early molecular mechanisms of this deregulation are unclear. To address this issue, we have defined the genome-wide PR and GATA2 cistrome in the murine uterus using chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-seq). In uteri of ovariectomized mice, we identified 6367 PR binding sites in the absence of P4 ligand; however, this number increased at nearly three fold (18,432) following acute P4 exposure. Sequence analysis revealed that approximately 73% of these binding sites contain a progesterone response element (PRE) or a half-site motif recognized by the PR. Many previously identified P4 target genes known to regulate uterine function were found to contain PR binding sites, confirming the validity of our methodology. In addition we identified 46,183 GATA2 binding sites in P4 treatment conditions with 7,954 binding sites overlapping that of the PR. Gene expression data from ovariectomized Oil and P4 treated Gata2 f/f uterus horn
2012-09-06 | E-GEOD-34902 | biostudies-arrayexpress
Project description:We generated homozygous GATA2 knockout human embryonic stem cells (GATA2-/- hESCs) and analyzed their blood differentiation potential. Paritcularly at the hemogenic endothelium (HE) stage and hematopoietic progenitor cell (HPC) stage. Our result revealed that GATA2-/- hESCs displayed attenuated generation of CD34+CD43+ HPCs, due to the impairment of endothelial to hematopoietic transition (EHT). However, GATA2-/- hESCs retained the potential to generate erythroblasts, macrophages, but never granulocytes. Through RNA-Seq and further rescue experiment, we further identified that SPI1 was responsible for the defect of GATA2-/- hESCs in generation of CD34+CD43+ HPCs and granulocytes.
2017-02-09 | GSE69797 | GEO
Project description:Progesterone (P4) signaling through its nuclear transcription factor, the progesterone receptor (PR), is essential for normal uterine function. Although deregulation of PR mediated signaling is known to underscore uterine dysfunction and a number of endometrial pathologies, the early molecular mechanisms of this deregulation are unclear. To address this issue, we have defined the genome-wide PR and GATA2 cistrome in the murine uterus using chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-seq). In uteri of ovariectomized mice, we identified 6367 PR binding sites in the absence of P4 ligand; however, this number increased at nearly three fold (18,432) following acute P4 exposure. Sequence analysis revealed that approximately 73% of these binding sites contain a progesterone response element (PRE) or a half-site motif recognized by the PR. Many previously identified P4 target genes known to regulate uterine function were found to contain PR binding sites, confirming the validity of our methodology. In addition we identified 46,183 GATA2 binding sites in P4 treatment conditions with 7,954 binding sites overlapping that of the PR. Examination of PR and Gata2 binding in whole or epithelial isolated mouse uterine tissue upon acute vehicle/P4 treatement
2012-09-06 | E-GEOD-34927 | biostudies-arrayexpress