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Gene expression by RNA sequenicng of extracellular vesicle labeled Granulocyte macrophage progenitors (GMPs) [mRNA]

ABSTRACT: Gene expression by RNA sequenicng of extracellular vesicle labeled Granulocyte macrophage progenitors (GMPs) [mRNA]

PROVIDER: PRJNA525656 | ENA |

REPOSITORIES: ENA

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Extracellular vesicle labeled Granulocyte macrophage progenitors

Project description:Extracellular vesicle labeled Granulocyte macrophage progenitors

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Small RNA sequencing of bone marrow extracellular vesicle labeled Granulocyte macrophage progenitors (GMPs) [GMP.sRNA]

Project description:Small RNA sequencing of bone marrow extracellular vesicle labeled Granulocyte macrophage progenitors (GMPs) [GMP.sRNA]

| PRJNA525665 | ENA

Small RNA sequencing of bone marrow extracellular vesicle labeled Granulocyte macrophage progenitors (GMPs) [GMP.sRNA]

Project description:Small RNA sequenicg was performed on mouse bone marrow GMPs (Lin-, cKit+, Sca1-, CD34+, CD16/32 hi) labeled by osteoblastic cell derived extracellular vesicles as indicated by GFP labeling. Cells were isolated by FACS sorting from the bone marrow of Ocn-GFPTopaz mice and total RNA was extracted using the miRNeasy micro kit from (Qiagen)

2021-12-08 | GSE127869 | GEO

Gene expression by RNA sequenicng of extracellular vesicle labeled Granulocyte macrophage progenitors (GMPs) [mRNA]

Project description:RNA sequenicg was performed on mouse bone marrow GMPs (Lin-, cKit+, Sca1-, CD34+, CD16/32 hi) labeled by osteoblastic cell derived extracellular vesicles as indicated by GFP labeling. Cells were isolated by FACS sorting from the bone marrow of Ocn-GFPTopaz mice and total RNA was extracted using the miRNeasy micro kit from (Qiagen)

2021-12-08 | GSE127858 | GEO

Extracellular vesicle labeled Granulocyte macrophage progenitors

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-08 | GSE127872 | GEO

RNA-seq of mouse myeloid progenitors reveals two independent pathways for monocyte production via GMPs and MDPs

Project description:Granulocyte-monocyte progenitors (GMPs) and monocyte-dendritic cell progenitors (MDPs) produce monocytes during homeostasis and in response to increased demand during infection. Both progenitor populations are thought to derive from common myeloid progenitors (CMPs), and a hierarchical relationship (CMP-GMP-MDP-monocyte) is presumed to underlie monocyte differentiation. Here, however, we demonstrate that mouse MDPs arose from CMPs independently of GMPs, and that GMPs and MDPs produced monocytes via similar, but distinct, monocyte-committed progenitors. GMPs and MDPs yielded classical (Ly6Chi) monocytes with gene expression signatures that were defined by their origins and impacted their function. GMPs produced a subset of “neutrophil-like” monocytes, whereas MDPs gave rise to a subset of monocytes that yielded monocyte-derived dendritic cells. GMPs and MDPs were also independently mobilized to produce specific combinations of myeloid cell types following the injection of microbial components. Thus, the balance of GMP and MDP differentiation shapes the myeloid cell repertoire during homeostasis and following infection.

2017-11-21 | GSE88982 | GEO

scRNAseq reveals heterogeneity among mouse bone marrow Ly6Chi monocytes produced by GMPs and MDPs

2017-11-13 | GSE104478 | GEO

Effect of Dot1l deletion on LSKs and GMPs

Project description:We wanted to investigate the effects of Dot1l deletion on gene expression in LSKs and GMPs of C57/BL6 mice Aberrant Hox gene activation is a recurrent feature in several different types of human leukemia, including leukemias with rearrangements of the mixed lineage leukemia (MLL) gene. In this study, we demonstrate that Hox gene expression is controlled by higher degree H3K79 methylation in acute myeloid leukemia (AML). We show that the deposition of progressive H3K79 methylation states at the genomic loci of critical Hox genes is dependent on the interaction of the H3K79 methyltransferase Dot1l with Af10, a protein that is found in the Dot1l complex isolated from diverse cell types. Furthermore, abrogation of the Dot1l-Af10 interaction reverses aberrant epigenetic profiles found in the leukemia epigenome and impairs the transforming ability of mechanistically distinct AML oncogenes. Lineage negative Sca-1 positive Kit positive (LSK) cells and granulocyte macrophage progenitors (GMPs) were sorted from Dot1 wt/wt x Mx-Cre mice or Dot1l fl/fl x Mx-Cre mice were injected with PIPC. PIPC injection induced biallelic deletion of the Dot1l allele in the Dot1l fl/fl mice but not the Dot1l wt/wt mice. The Dot1l wt/wt LSKs and GMPs were compared to the Dot1l -/- counterparts by RNA extraction and Microarrays.

2014-09-08 | E-GEOD-54498 | biostudies-arrayexpress

Microarray data from L-GMPs and GMPs

Project description:A leukemia cell fraction highly enriched for LSCs was generated in a mouse model of AML induced by co-expression of MLL target genes Hoxa9 and Meis1. Limit dilution transplantation analyses performed on various prospectively isolated leukemia cell subpopulations revealed that cells capable of transplanting AML to syngeneic recipient mice (the operational definition of LSCs) were highly enriched in the leukemia cell fraction displaying an immunophenotype (Lin- Sca1- c-kit+ CD16/32+ CD34+) comparable to normal GMPs, referred to as L-GMPs. For the purpose of identifying genes that are differentially expressed in LSCs, microarray expression profiling was performed on L-GMPs (from leukemic mice) and GMPs (from normal mouse BM) purified by flow cytometry.

2015-10-02 | GSE64773 | GEO

Expression data from bone marrow derived granulocyte monocyte precursors (GMPs) from wt -, Gfi1 knock-out -, human-Gfi1-SNP36N knock in and human wt-Gfi1 knock in mice

Project description:The incidence of cancer is not only influenced by exposure to environmental factors such as toxic substances and chemotherapy, but is also a result of individual predispositions. Single Nucleotide Polymorphisms (SNPs) represent one such individual predisposition to cancer1. Gfi136N is a SNP in the coding region of the gene “Growth factor independence 1 (Gfi1)” predisposing to development of Acute myeloid leukemia (AML). However, the mechanisms how this polymorphism is associated with AML are unknown. Here we present a mouse model in which the presence of Gfi136N leads to altered epigenetic modifications in the myeloid progenitor fraction “Granulocytic Monocytic Progenitor (GMP)” and demonstrates how this might predispose to AML. Presence of Gfi136N leads to a different epigenetic programming of the GMPs resulting in higher levels of the leukemogenic transcription factor Hoxa9. To our knowledge, this is the first mouse model of a SNP leading to epigenetic changes. Thus, SNPs not only result in an altered structure or expression level of certain proteins but here we show that SNPs might also lead to different cancer related epigenetic modifications. We used microarrays to detail the changes in the program of gene expression of GMPs induced by the knock in of human Gfi1 variants in the mouse Gfi1 locus Bone marrow derived granulocyte monocyte precursors (GMPs) from wt.-,Gfi1 knock-out.-, human Gfi1-knock in and human Gfi1-SNP36N knock in mice were collected by fluorescence activated cell sorting (FACS) for total RNA extraction and gene expression analysis on affymetrix mouse Gene 1.0 ST arrays. We aimed to identify differentially regulated target genes of the human Gfi1-SNP36N variant in a mouse model system which mit contribute to the development of acute myeloid leukemia (AML).

2012-11-22 | E-GEOD-25551 | biostudies-arrayexpress

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