Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from Bone marrow and Fetal liver Lineage-c-Kit+Sca-1+ (LSK) cells

ABSTRACT: Loss of polycomb-group gene Ezh2 causes activation of fetal gene signature in adult mouse bone marrow (BM) hematopoietic stem and progenitor cells (HSPCs). Ezh2 directly represses fetal-specific let-7 target genes, including Lin28, thereby cooperates with let-7 microRNAs in silencing fetal gene signature in BM HSPCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE69760 | GEO | 2015/08/27

SECONDARY ACCESSION(S): PRJNA286674

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from Bone marrow and Fetal liver Lineage-c-Kit+Sca-1+ (LSK) cells

Project description:Loss of polycomb-group gene Ezh2 causes activation of fetal gene signature in adult mouse bone marrow (BM) hematopoietic stem and progenitor cells (HSPCs). Ezh2 directly represses fetal-specific let-7 target genes, including Lin28, thereby cooperates with let-7 microRNAs in silencing fetal gene signature in BM HSPCs. We purified Lineage-Sca-1+c-Kit+ (LSK) HSPCs from E14.5 FL and adult BM and subjected them to microarray analysis.

2015-08-27 | E-GEOD-69760 | biostudies-arrayexpress

Expression data from Tet2-hypomorph (knockdown) and/or Ezh2-null Lineage-Sca-1+c-Kit+ (LSK) cells and granulocyte-macrophage progenitors (GMPs)

Project description:PcG proteins form the polycomb repressive complexes (PRC) 1 and 2, functioning as transcriptional repressors through histone modifications. They have been implicated in the maintenance of self-renewing somatic and cancer stem cells. PcG genes have been characterized as tumor suppressor genes as exemplified by somatic inactivating mutations of EZH2, a gene encoding histone methyltransferase in PRC2, in myeloid malignancy. Mice deficient for Tet2 have been reported to recapitulate some aspects of myeloid malignancies. We evaluated the Ezh2-deficient mice and also tested the impact of concurrent depletion of Ezh2 and Tet2 on hematopoiesis. Purified LSK cells and GMPs from BM of recipient mice repopulated with wild-type, Tet2KD/KD, Ezh2-/- and Tet2KD/KDEzh2-/- fetal liver cells were subjected to RNA extraction and hybridization on Agilent microarrays.

2013-08-01 | E-GEOD-42666 | biostudies-arrayexpress

Expression data from diseased Ezh2 KO Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

Project description:Recent studies have shown that epigenetic regulator are mutated in myelodysplastic syndrome (MDS) patients. Ezh2 is frequently mutated in hematopoietic malignant patients, however, the pathophysiological role of Ezh2 mutations has not been elucidated yet. In this study, we examined the function of Ezh2 in murine hematopoietic disease. Ezh2 deleted mice with myeloid malignancies including MDS, Myelodysplasia/myeloneoplasm(MDS/MPN), Myelodysplasia/myeloneoplasm_thrombocytosis(MDS/MPN_TC)

2015-03-14 | GSE66897 | GEO

Expression data from cultured c-Kit+Sca-1+Lin- (KSL)cells

2012-07-04 | GSE39082 | GEO

Expression data from RUNX1S291fs-mutant and/or Ezh2 conditional knockout Lineage-c-Kit+Sca-1+ (LSK) cells

2013-09-04 | GSE50537 | GEO

Expression data from cultured c-Kit+Sca-1+Lin- (KSL)cells

Project description:The Notch signaling pathway plays a critical role in regulating the proliferation and differentiation of stem and progenitor cells including hematopoietic stem and progenitor cells (HSPCs). Notch receptors and ligands are expressed in BM stromal and hematopoietic cells. A large body of evidence has demonstrated that activating Notch signaling enhances HSCs self-renewal and facilitates its expansion ex vivo. We report that an endothelium-targeted soluble Notch ligand, the DSL domain of mouse Delta-like 1 fused with a RGD motif (mD1R), efficiently promotes the expansion ex vivo of mouse bone marrow HSPCs in a Notch signaling and endocytosis dependent manner. HSPCs expanded in the presence of mD1R kept long-term HSPC repopulation capacity. We used microarrays to compare the gene expression profiles of HSPCs expanded in the presence of PBS and mD1R. KSL cells were plated on Human umbilical vein endothelial cells (HUVECs) and cultured in a serum-free medium supplemented with a cocktail containing 5 types of mouse cytokines (m5GF) in the presence of PBS or mD1R for 7 days. Then KSL cells were sorted from these cultured hematopoietic cells for RNA extraction and hybridization on Affymetrix microarrays. The experiments were repeated 3 times.

2012-07-03 | E-GEOD-39082 | biostudies-arrayexpress

Expression data from RUNX1S291fs-mutant and/or Ezh2 conditional knockout Lineage-c-Kit+Sca-1+ (LSK) cells

Project description:Recent studies have showed that loss-of-function mutations of EZH2, a catalytic component of polycomb repressive complex 2, are often associated with RUNX1 mutations in myelodysplastic syndrome (MDS) patients. We established a novel MDS model mouse by transducing a RUNX1S291fs mutant in hematopoietic stem cells followed by deletion of Ezh2 and found that Ezh2 loss significantly promoted RUNX1S291fs-induced MDS. We retrovirally transduced RUNX1S291fs or empty-control into either Cre-ERT;Ezh2wt/wt or Cre-ERT;Ezh2flox/flox (CD45.2+) HSCs. The transduced cells were transplanted into lethally irradiated recipient mice together with life-saving CD45.1+ wild-type bone marrow cells. After deletion of Ezh2, gene expression analysis were performed on pooled bone marrow LSK cells isolated from WT, Ezh2Δ/Δ, RUNX1S291fs, and RUNX1S291fs/Ezh2Δ/Δ mice (n=2-4) and two distinct RUNX1S291fs/Ezh2Δ/Δ-MDS mouse.

2013-09-04 | E-GEOD-50537 | biostudies-arrayexpress

H3K27me3 ChIP-sequencing on LSK (Lin-Sca-1+c-kit+) cells isolated from control, MxCre Jak2VF/+ and MxCre Jak2VF/+ EZH2-/- mice

Project description:Inactivating EZH2 mutations have been associated with myelofibrosis (MF). Moreover, EZH2 mutations co-exist with the JAK2V617F mutation in a significant cases of MF. To determine the effects of concomitant loss of EZH2 and JAK2V617F mutation in hematopoiesis, we generated Ezh2-deficient Jak2V617F-expressing mice. To identify the Ezh2 target genes that are regulated by H3K27me3 in MF, we performed H3K27me3 ChIP-sequencing in sorted LSK cells from control, MxCre;Jak2VF/+ and MxCre;Jak2VF/+ EZH2-/- mice.

2016-04-19 | GSE79319 | GEO

Murine fetal bone marrow does not support functional hematopoietic stem and progenitor cells until birth

Project description:Fetal hematopoietic stem and progenitor cells (HSPCs) migrate from fetal liver (FL) to bone marrow (BM) around birth. While adult BM HSPCs and their extrinsic regulation is well studied, little is known about the composition, function, and extrinsic regulation of the first HSPCs to enter the BM. Here, we show that HSPCs colonize multiple fetal bones by E15.5, shift from an MPP2 to an MPP3/4-dominant phenotype by birth, and display little function until E18.5, relative to their FL counterparts. We establish a transcriptional atlas of single perinatal HSPCs, and their putative BM niches, from E15.5 through P0 and show that early fetal BM (FBM) lacks HSPCs with intrinsic stem cell programs and niche cells supportive of HSPCs. In contrast, stem cell programs are preserved in neonatal BM HSPCs, which engage with a niche expressing HSC supportive factors distinct from those seen in adult BM (i.e., IGF).

2021-06-26 | GSE178951 | GEO

Expression data from Lineage-c-Kit+Sca-1+ (LSK) and megakaryocyte/erythroid progenitor (MEP) cells isolated from JAK2V617F/Ezh2Δ/Δ mice post JQ1 treatment

Project description:Loss-of-function mutations in EZH2 are associated with worse outcomes in patients with primary myelofibrosis (PMF). To understand how EZH2 insufficiency is involved in the pathogenesis of PMF, we generated mice compound for Ezh2 conditional deletion and a JAK2V617F transgene.

2015-06-04 | GSE69499 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data