E-GEOD-18061
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA119327
PROVIDER: E-GEOD-18061 | ExpressionAtlas | 2014-07-03
REPOSITORIES: ExpressionAtlas
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Project description:miR-125a knockout mice develop myeloproliferave disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+) and (+/-) MPD mice was performed using CodeLink Whole Genome DNA array analysis. Codelink Mouse Whole Genome Bioarrays were performed according to the manufacturer’s instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with MPD. One replicate per array.
2015-06-30 | E-GEOD-65648 | biostudies-arrayexpress
Project description:miR-125a knockout mice develop myeloproliferative disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+), (+/-) MPD, and (-/-) MPD mice was performed by using CodeLinkTM Whole Genome DNA array analysis. CodeLink Mouse Whole Genome Bioarrays were performed according to the manufacturerâs instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mouse, miR-125a (+/-) heterozygous mouse with MPD, and miR-125a (-/-) homozygous mouse with MPD. One replicate per array.
2015-12-31 | E-GEOD-69621 | biostudies-arrayexpress
Project description:To investigate the role of the transcription factor ERG in hematopoiesis we generated Erg heterozygous knockout and conditional Erg knockout mice. We found that several hematopoietic cell types were decreased in these mice. To define Erg downstream target genes in hematopoietic stem cells, we sorted Lineage-, Sca-1+, c-kit+, CD150+, CD48- cells from Erg +/- mice for gene expression analysis. To define Erg downstream target genes in hematopoietic progenitors, we sorted multipotent progenitors (Lineage-, Sca-1+, c-kit+, CD150-) from Erg -/- mice for gene expression analysis. We generated Erg heterozygous knockout mice and provide 3 replicates for wild type (Erg +/+) populations of stem cells (HSC) and 3 replicates for Erg +/- mices. We also generated a conditional Erg knockout mice. We provide 3 replicates for Erg fl/fl and 3 replicates for Erg (-/-) mice.
2015-09-21 | E-GEOD-69873 | biostudies-arrayexpress
Project description:To investigate the role of the transcription factor ERG in hematopoiesis we generated Erg heterozygous knockout and conditional Erg knockout mice. We found that several hematopoietic cell types were decreased in these mice. To define Erg downstream target genes in hematopoietic stem cells, we sorted Lineage-, Sca-1+, c-kit+, CD150+, CD48- cells from Erg +/- mice for gene expression analysis. To define Erg downstream target genes in hematopoietic progenitors, we sorted multipotent progenitors (Lineage-, Sca-1+, c-kit+, CD150-) from Erg -/- mice for gene expression analysis.
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Project description:T cell development is accompanied by epigenetic changes that ensure the silencing of stem cell-related, and the activation of lymphocyte-specific programs. How transcription factors influence these changes remains unclear. We show that the Ikaros transcription factor interacts with the Polycomb Repressive Complex 2 (PRC2) in CD4-CD8- thymocytes, and allows its binding to >200 developmentally-regulated genes, many of which are expressed in hematopoietic stem cells. Loss of Ikaros in CD4-CD8- cells leads to diminished histone H3 Lys27 (H3K27) trimethylation and ectopic expression of these genes. Ikaros binding triggers PRC2 recruitment and H3K27 trimethylation. Furthermore, Ikaros interacts with PRC2 independently of the Nucleosome Remodeling and Deacetylation complex. Our results identify Ikaros as a fundamental regulator of PRC2 function in developing T cells. Genome-wide comparison of different histone modifications, Ikaros, Suz12 and NuRD binding in different stages of T cell development in WT and Ikaros mutant mice. Profiling of H3K27me3 in DN1, DN2, DN3, DN4 and DP thymocytes and hematopoietic stem and progenitor cells (LSK cells) of WT and Ikaros mutant mice. Profiling of H3K4me3 and H3ac in WT and Ikaros mutant DP thymocytes. Global analysis of Ikaros binding in WT DN3, DN4 and DP cells, Suz12 binding in WT and Ikaros mutant DN3 cells, and Mta2 and Mi2beta binding in WT DN3 cells. Genome-wide profiling of Ikaros binding and H3K27me3 upon Ikaros activation in Ikaros-deficient leukemic T cells.
2015-11-03 | E-GEOD-61148 | biostudies-arrayexpress
Project description:In vertebrates, lifelong supply of all the blood cell types in suitable numbers is maintained by the hematopoietic stem cells (HSCs). During development, these HSCs emerge in the aorta-gonad-mesonephros (AGM) from specialized vascular endothelium through a transdifferentiation process, called as endothelial-to-hematopoietic transition (EHT). During this process, select endothelial cells (CD31+c-kit- or CD31PCKITN) switch to a hematopoietic transcriptional program, undergo morphological changes and become hemogenic (CD31+c-kit+ or CD31PCKITP) and gives rise to hematopoietic cells (CD31-c-kit+ or CD31NCKITP). A complex interplay of key transcription factors and signaling pathways coordinates the whole process. Specific metabolic signature of a cell can precisely define its phenotype. Evidence has emerged that cellular phenotype and function can be driven according to the changes in cellular metabolism. Metabolic programs, which are stage specific, allow stem cells to adapt their function in different microenvironments. In the present study, we performed nano LC-MS/MS based proteomic analysis to understand the molecular program involved in the transdifferentiation of endothelial to hematopoietic cells.
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2016-02-04 | E-MTAB-4133 | biostudies-arrayexpress
Project description:<p>We are studying the natural history, pathogenesis and treatment of patients with WHIM syndrome, an immunodeficiency disorder characterized by warts, hypogammaglobulinemia, recurrent infections and neutropenia usually due to autosomal dominant gain-of-function mutations in chemokine receptor <i>CXCR4</i>. We have identified a patient born with WHIM syndrome and the WHIM mutation <i>CXCR4<sup>R334X</sup></i> who has been disease-free for 20 years and who lacks <i>CXCR4<sup>R334X</sup></i> in myeloid cells, the cells that drive disease manifestations. She is a genetic and hematopoietic mosaic, since she still has the mutation in lymphoid cells and non-hematopoietic cells. Cytogenetics and microarray analysis revealed that the mechanism of loss of the mutation was deletion of the mutant allele from one copy of chromosome 2. Whole genome sequencing of patient neutrophil and skin fibroblast genomic DNA revealed that the mechanism of deletion was chromothripsis, a process of chromosome shattering resulting in deletions and rearrangements of the non-deleted chromosomal segments. In the patient, this process evidently occurred in a single hematopoietic stem cell (HSC), resulting in deletion of the disease allele <i>CXCR4<sup>R334X</sup></i> and one copy of 163 other genes on chromosome 2. This HSC evidently acquired a growth advantage and repopulated the HSC population and the myeloid lineage. Consistent with this, studies using gene targeted mice in competitive bone marrow transplantation experiments revealed that selective <i>Cxcr4</i> haploinsufficiency (inactivation of one copy of <i>Cxcr4</i> and not of any other genes) was sufficient to confer a strong engraftment advantage over bone marrow cells from wild type mice as well as bone marrow cells from a mouse model of WHIM syndrome. These results suggest that <i>CXCR4</i> knockdown may be a useful strategy to enhance bone marrow engraftment in the absence of toxic bone marrow conditioning regimens.</p>
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Project description:Long-term hematopoietic stem cells are rare, highly quiescent stem cells of the hematopoietic system with life-long self-renewal potential and the ability to transplant and reconstitute the entire hematopoietic system of conditioned recipients. Most of our understanding of these rare cells has relied on cell surface identification, epigenetic and transcriptomic analyses. Our knowledge of protein synthesis, folding, modification and degradation – broadly termed protein homeostasis or “proteostasis” – in these cells is still in its infancy. Here we report the requirement of the small phospho-binding adaptor proteins, the cyclin dependent kinase subunits (Cks1 and Cks2), for maintaining ordered hematopoiesis and long-term hematopoietic stem cell reconstitution. Cks1 and Cks2 are critical regulators of a myriad of key intracellular signalling pathways that govern hematopoietic stem cell biology and together they balance protein homeostasis and restrain reactive oxygen species to ensure healthy hematopoietic stem cell function.
2023-03-11 | PXD035984 | Pride
Project description:miR-125a knockout mice develop myeloproliferave disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+) and (+/-) MPD mice was performed using CodeLink Whole Genome DNA array analysis.
2015-06-30 | GSE65648 | GEO