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RNAseq of granulocyte-macrophage progenitors (GMP) from bone marrow of mice with hematopoietic knock-out of Rnaseh2b

ABSTRACT: RNAseq of granulocyte-macrophage progenitors (GMP) from bone marrow of mice with hematopoietic knock-out of Rnaseh2b

PROVIDER: PRJNA857021 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20048850_1.fastq.gz	Fastqsanger.gz
	SRR20048850_2.fastq.gz	Fastqsanger.gz
	SRR20048851_1.fastq.gz	Fastqsanger.gz
	SRR20048851_2.fastq.gz	Fastqsanger.gz
	SRR20048852_1.fastq.gz	Fastqsanger.gz

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RNAseq of granulocyte-macrophage progenitors (GMP) from bone marrow of mice with hematopoietic knock-out of Rnaseh2b

Project description:Bulk transcriptomes of granulocyte-macrophage progenitor cells isolated from bone marrow of Rnaseh2bfl/fl/ Vav-Cre and Cre-negative ctrl mice; The sorted bone marrow cells had the following immunophenotype: lineage- CD201 (EPCR)- CD117+ CD16/32+ CD34+

2023-05-30 | GSE207761 | GEO

AML patient granulocyte macrophage progenitor (GMP) cells

Project description:AML patient granulocyte macrophage progenitor (GMP) cells

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Transcription profiling of mouse erythroid progenitors (EP) in comparison to granulocyte/monocyte - macrophage progenitors (GMP) from 10 - 16 week old C57/Bl6 - S129Ola

Project description:Mouse erythroid progenitors (EP) in comparison to granulocyte/monocyte - macrophage progenitors (GMP) from 10 - 16 week old C57/Bl6 - S129Ola (mixed genetic background) purified by flow cytometry

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Molecular reprogramming of granulocyte/macrophage progenitor (GMP) clusters

Project description:Molecular reprogramming of granulocyte/macrophage progenitor (GMP) clusters

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Project description:AML patient granulocyte macrophage progenitor (GMP) cells [human]

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Mouse inv(16):TET2ko granulocyte macrophage progenitor (GMP) cells

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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).

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Transcription profiling of human HSC enriched population, common myeloid progenitors, granulocyte macrophage progenitors, megakaryocyte progenitors, and leukemia stem cells (leukemic-GMP) reveals MLL-AF9 transforms committed progenitors to leukemia stem cells by activation of a stem cell program (expt 2)

Project description:Leukemias and other cancers possess a rare population of cells capable of self-renewal, and eradication of these cancer stem cells is likely necessary for long-term cancer-free survival. Given that both normal and cancer stem cells are capable of self-renewal the extent to which cancer stem cells resemble normal tissue stem cells is a critical issue if targeted therapies are to be developed. We introduced the MLL-AF9 fusion protein encoded by the t(9;11)(p22;q23) found in human acute myelogenous leukemia (AML) into murine committed granulocyte-macrophage progenitors (GMP). The resultant leukemias contained cells with an immunophenotype similar to normal GMP that were highly enriched for leukemia stem cells (LSC). Detailed gene expression comparisons between normal hematopoietic stem cells (HSC), committed progenitors, and the LSC population demonstrated the LSC were globally more similar to the normal GMP than any other population. However, a subset of genes highly expressed in normal stem cells was re-activated in the LSC. These data demonstrate LSC can be generated from committed progenitors without widespread reprogramming of gene expression, and a leukemia self-renewal associated signature is activated in the process. Our findings define progression from normal hematopoietic progenitor to leukemia stem cell, and suggest that targeting a self-renewal program expressed in an abnormal context may be possible. Experiment Overall Design: A normal HSC enriched population, common myeloid progenitors, granulocyte macrophage progenitors, megakaryocyte progenitors, and leukemia stem cells (leukemic-GMP) were isolated and labeled RNA was hybridzed to Affymetrix microarrays

2008-06-12 | E-GEOD-3722 | biostudies-arrayexpress

EP - GMP

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WT and inv(16)/KITD816Y granulocyte macrophage progenitor (GMP) cells [mouse]

Project description:WT and inv(16)/KITD816Y granulocyte macrophage progenitor (GMP) cells [mouse]

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