Mus musculus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Similar Datasets
Project description:ChIP-seq for Fbxl10 in HSCs (Ly6A/Sca-1 Fbxl10 Tg vs Ctrl)
| PRJDB3904 | ENA
Project description:mRNA profiling of mouse spleens comparing wild type spleens vs. spleens from mice having deletion of RBP-J in cells of the renin lineage which results in B-cell leukemia We used microarrays to detail the global program of gene expression in wild type and the leukemic spleens which revealed upregulation of genes for cell cycle progression and B cell identity in the leukemic spleens.
2014-02-17 | GSE46229 | GEO
Project description:Stem cells antigen-1 (Sca-1) is an 18-kDa mouse glycosyl phosphatidylinositol-anchored cell surface protein that has widely been used for isolation of murine hematopoietic stem cells (HSCs). However, recently several studies have reported the expression of this protein in non-HSCs such as the liver, skin and muscles among others. In the current study, we used fluorescence-activated cell sorting (FACS) technique to sort Sca-1+ stem cells from mouse hindlimb muscles. The Sca-1+ cells were divided into two sets first set of Sca-1+ cells were processed for protein extraction immediately after sorting (ex vivo set) while the second set of samples, referred to as in vitro set, were expanded in cell culture after sorting and harvested after two passage and then processed for protein extraction. A high-resolution proteome map of the ex vivo and in vitro sets was generated Orbitrap Fusion Tribrid Mass Spectrometer. In total, the analysis led to the identification of 5,581 protein groups.
2021-06-21 | PXD022247 | Pride
Project description:mRNA profiling of mouse spleens comparing wild type spleens vs. spleens from mice having deletion of RBP-J in cells of the renin lineage which results in B-cell leukemia We used microarrays to detail the global program of gene expression in wild type and the leukemic spleens which revealed upregulation of genes for cell cycle progression and B cell identity in the leukemic spleens. Two condition experiment: wild type vs leukemic; biological replicates: individual mice - 2 wild type, 2 mutant. One replicate per array.
2014-02-17 | E-GEOD-46229 | biostudies-arrayexpress
Project description:Transcriptome analysis of leukemic granulocyte/macrophage progenitors (L-GMPs) from MLL-AF9-transduced Fbxl10+/+ and Fbxl10-/- cells (Fbxl10-/- L-GMPs vs Fbxl10+/+ L-GMPs)
| PRJDB5603 | ENA
Project description:Leukemic splenocytes from these commercial transgenic mice that developed fatal leukemia with massive splenomegaly were isolated at the time of the necropsy and subjected to gene expression profiling and phosphoprotein profiling in side by side comparison with CD22DE12-Tg BPL or CD22DE12_BCR-ABL double transgenic cells. Mouse leukemia cells were isolated from markedly enlarged spleens of CD22DE12-Tg (N=2), BCR-ABL-Tg (N=2), Eµ-MYC Tg mice (N=2) and Splenocytes from wildtype healthy C57BL/6 mice served as controls (N=4).
2015-06-25 | E-GEOD-58872 | biostudies-arrayexpress
Project description:Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNα), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFNα treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFNα target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-α/β receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFNα stimulation, demonstrating that STAT1 and Sca-1 mediate IFNα induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFNα and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFNα are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFNα pathway in HSCs impairs their function, acute IFNα treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNα on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells. cDNA microarray analysis was performed on sorted Lin neg, cKit+, CD150+, CD48neg HSCs from IFNα treated (16h after treatment) and untreated (littermate) mice. Per condition 3 independent biological replicates were analysed.
2009-01-15 | E-GEOD-14361 | biostudies-arrayexpress
Project description:We compared gene expression differences in Atxn1L knockout vs wildtype HSCs KO allele described in Pub Med ID: 22014525 HSCs were purified as Lineage-negative, Sca-1+ c-Kit+ (LSK), CD150+ and Side population from both Atxn1L-null and WT mice on C57Bl/6 background
2013-02-28 | E-GEOD-44285 | biostudies-arrayexpress
Project description:Single cell whole transcriptome analysis of young (2-3 months) and old (20-25 months) mouse HSCs, defined as Linâ??Sca-1+c-Kit+150+CD48â?? . Differential gene expression analysis of young and old mouse HSCs (Linâ??Sca-1+c-Kit+150+CD48â?? )
2016-03-24 | E-GEOD-70657 | biostudies-arrayexpress
Project description:Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNα), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFNα treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFNα target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-α/β receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFNα stimulation, demonstrating that STAT1 and Sca-1 mediate IFNα induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFNα and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFNα are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFNα pathway in HSCs impairs their function, acute IFNα treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNα on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells.
2009-01-15 | GSE14361 | GEO