Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA105243 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series:; GSE9188: Differentially regulated genes in LT-HSC from control or Pbx1-null mice; GSE9189: Differentially regulated genes in normal LT-HSC vs ST-HSC Experiment Overall Design: Refer to individual Series
2008-06-20 | E-GEOD-9198 | biostudies-arrayexpress
Project description:Differentially regulated genes in normal LT-HSC vs ST-HSC
| PRJNA105245 | ENA
Project description:Self-renewal is a defining characteristic of stem cells, however the molecular pathways underlying its regulation are poorly understood. Here we demonstrate that conditional inactivation of the Pbx1 proto-oncogene in the hematopoietic compartment results in a progressive loss of long-term hematopoietic stem cells (LT-HSCs) that is associated with concomitant reduction in their quiescence, leading to a defect in the maintenance of self-renewal as assessed by serial transplantation. Transcriptional profiling revealed that multiple stem cell maintenance factors are perturbed in Pbx1-deficient LT-HSCs, which prematurely express a large subset of genes, including cell cycle regulators, normally expressed in non-self-renewing multipotent progenitors. A significant proportion of Pbx1-dependent genes are associated with the Tgf-b pathway, which serves a major role in maintaining HSC quiescence. Pbx1-deficient LT-HSCs are unable to up-regulate the cyclin dependent kinase inhibitor p57 in response to Tgf-b, providing a mechanism through which Pbx1 maintenance of stem cell self-renewal is achieved. Experiment Overall Design: Highly efficient Pbx1 deletion was induced with poly(I:C) in 3 young MxCre+.Pbx1f/f mutant or 2 MxCre-.Pbx1f/f control mice. LT-HSC (Lin-cKit+Sca1+CD34-CD135-) cells were prospectively sorted from bone marrow of individual mice harvested 4 weeks after the last injection of poly(I:C).
2008-06-20 | E-GEOD-9188 | biostudies-arrayexpress
Project description:Self-renewal is a defining characteristic of stem cells, however the molecular pathways underlying its regulation are poorly understood. Here we demonstrate that conditional inactivation of the Pbx1 proto-oncogene in the hematopoietic compartment results in a progressive loss of long-term hematopoietic stem cells (LT-HSCs) that is associated with concomitant reduction in their quiescence, leading to a defect in the maintenance of self-renewal as assessed by serial transplantation. Transcriptional profiling revealed that multiple stem cell maintenance factors are perturbed in Pbx1-deficient LT-HSCs, which prematurely express a large subset of genes, including cell cycle regulators, normally expressed in non-self-renewing multipotent progenitors. Experiment Overall Design: LT-HSC (Lin-cKit+Sca1+CD34-CD135-) and ST-HSC (Lin-cKit+Sca1+CD34+CD135-) cells were prospectively sorted from the BM of MxCre-.Pbx1f/f control mice harvested 4 weeks after the last injection of poly(I:C).
2008-06-20 | E-GEOD-9189 | biostudies-arrayexpress
Project description:Differentially regulated genes in control and c-myc N-myc deficient LT-HSCs
| PRJNA114221 | ENA
Project description:Self-renewal is a defining characteristic of stem cells, however the molecular pathways underlying its regulation are poorly understood. Here we demonstrate that conditional inactivation of the Pbx1 proto-oncogene in the hematopoietic compartment results in a progressive loss of long-term hematopoietic stem cells (LT-HSCs) that is associated with concomitant reduction in their quiescence, leading to a defect in the maintenance of self-renewal as assessed by serial transplantation. Transcriptional profiling revealed that multiple stem cell maintenance factors are perturbed in Pbx1-deficient LT-HSCs, which prematurely express a large subset of genes, including cell cycle regulators, normally expressed in non-self-renewing multipotent progenitors. A significant proportion of Pbx1-dependent genes are associated with the Tgf-b pathway, which serves a major role in maintaining HSC quiescence. Pbx1-deficient LT-HSCs are unable to up-regulate the cyclin dependent kinase inhibitor p57 in response to Tgf-b, providing a mechanism through which Pbx1 maintenance of stem cell self-renewal is achieved. Keywords: genetic modification
2008-05-07 | GSE9188 | GEO
Project description:We analyzed the transcriptome of LT-HSCs sorted from wildtype and DERARE knockout mice. We aim at identifying differentially expressed genes and downstream signaling pathways associated with HSC defects in DERARE KO mice, and determining whether Wnt5a treatment could rescue the HSC defects in DERARE KO mice.
2018-05-29 | GSE87556 | GEO
Project description:Here we addressed the mRNA transcriptome of Long-Term Hematopoietic Stem Cells (LT-HSC) and Multipotent Progenitor (MPP) -3 and -4 purified from WT and Helios KO mice. By analyzing the differentially expressed genes among WT and KO condition we found that Helios deletion affects transcription mostly in the LT-HSC compartment and favor a megakaryocyte mRNA lineage priming at the expense of the lymphoid one.
2021-08-13 | GSE149244 | GEO
Project description:Expression data from control and Pbx1-null CMPs and GMPs
| PRJNA144049 | ENA
Project description:Here we tracked transcriptional changes in LT, ST-HSC and MLP after transplantation into immunocompromised mice. We show that LT- and ST-HSC activate similar pathways upon transplantation but they modulate distinct sets of genes. Total RNA was obtained from flow-sorted populations of human LT-, ST-HSC and MLP isolated from cord blood or immunocompromised mice transplanted with human at hematopoeitic progenitors at different time points after transplantation.
2015-02-20 | E-GEOD-58299 | biostudies-arrayexpress