Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA168600 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We used Affymetrix microarrays to characterize gene expression profiles that were perturbed in common myeloid progenitor (CMP) cells due to enforced expression of full-length or truncated forms of MN1. Expression profiles of MN1-induced leukemias arising from whole bone marrow transduction were also compared with the profiles obtained from the CMP cells. Lineage negative mouse bone marrow cells were transduced with retroviral vectors expressing full-length or truncated MN1 proteins. After 2 days in culture, cells were FACS-sorted for GFP expression and cultured for a further 3 days in growth media. After 5 days total, RNA was isolated and processed for microarray analysis. RNA was also prepared for microarray analysis from leukemias arising in mice following whole bone marrow transduction with full-lenght MN1.
2013-06-13 | E-GEOD-38767 | biostudies-arrayexpress
Project description:We used Affymetrix microarrays to characterize gene expression profiles that were perturbed in common myeloid progenitor (CMP) cells due to enforced expression of full-length or truncated forms of MN1. Expression profiles of MN1-induced leukemias arising from whole bone marrow transduction were also compared with the profiles obtained from the CMP cells.
2013-06-13 | GSE38767 | GEO
Project description:The molecular mechanism defining susceptibility of normal cells to oncogenic transformation may be a valuable therapeutic target. We characterized the cell of origin and its critical pathways in MN1 leukemias. Common myeloid (CMP), but not granulocyte-macrophage progenitors (CMP) could be transformed by constitutively overexpressed MN1. Complementation studies of CMP-signature genes in GMPs demonstrated that leukemogenicity of MN1 required the MEIS1/abdB-like HOX protein complex. Colocalization studies by ChIP-seq identified common chromatin targets of MN1 and MEIS1 that were associated with open chromatin and transcriptional activation. Transcriptional repression of MEIS1 target sites in established MN1 leukemias had antileukemic activity. As MN1 relies on but can not activate expression of MEIS1/abdB-like HOX proteins, transcriptional activity of these genes determines which cell is the cell of origin in MN1 leukemia. We have showed at the single cell level that CMPs, but not GMPs, are susceptible to MN1-induced transformation. To identify transcriptional differences between CMPs and GMPs that may explain this difference in susceptibilities to MN1 transformation we produced gene expression profiles (two biological replicates in each experimental arm) of bone marrow cells from MN1 leukemic mice and mature myeloid bone marrow cells (Gr1+/CD11b+) from healthy mice and compared those to already published gene expression profiles of CMPs and GMPs (Krivtsov, A.V., et al. (2006). Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9. Nature 442, 818-822).
2011-05-19 | E-GEOD-22923 | biostudies-arrayexpress
Project description:The molecular mechanism defining susceptibility of normal cells to oncogenic transformation may be a valuable therapeutic target. We characterized the cell of origin and its critical pathways in MN1 leukemias. Common myeloid (CMP), but not granulocyte-macrophage progenitors (CMP) could be transformed by constitutively overexpressed MN1. Complementation studies of CMP-signature genes in GMPs demonstrated that leukemogenicity of MN1 required the MEIS1/abdB-like HOX protein complex. Colocalization studies by ChIP-seq identified common chromatin targets of MN1 and MEIS1 that were associated with open chromatin and transcriptional activation. Transcriptional repression of MEIS1 target sites in established MN1 leukemias had antileukemic activity. As MN1 relies on but can not activate expression of MEIS1/abdB-like HOX proteins, transcriptional activity of these genes determines which cell is the cell of origin in MN1 leukemia.
2011-05-19 | GSE22923 | GEO
Project description:Glial pathology has been implicated as a causal contributor to the dysfunction and death of striatal neurons that characterizes Huntington disease. In this study, we investigated mutant HTT (mHTT)-associated changes in gene expression by both mouse and human striatal astrocytes. Mouse striatal astrocytes were FACS-sorted from two distinct models, R6/2 and zQ175 mice, which respectively express exon1-only truncated or full-length HTT, while human astrocytes were generated from either hESCs expressing full-length mHTT, or fetal striatal glia transduced with exon1-only mHTT. Comparison of differential gene expression between each of these conditions and their normal HTT controls, and to one another, revealed astrocyte-specific alterations in both truncated and full-length mHTT models that were shared by both species, yet with differences that clearly distinguished glia derived from each model. Overlap of these data sets revealed that the patterns of mHTT-associated transcriptional dysregulation depended not only upon species, but also upon whether the astroglia expressed truncated or full-length mHTT. These data revealed a common set of conserved, mHTT-associated dysregulated pathways that may present targets for the rescue of glial pathology in HD, while revealing that the gene expression of glia expressing truncated mHTT may differ substantially from that of glia expressing full-length mHTT.
2021-04-07 | GSE154131 | GEO
Project description:Glial pathology has been implicated as a causal contributor to the dysfunction and death of striatal neurons that characterizes Huntington disease. In this study, we investigated mutant HTT (mHTT)-associated changes in gene expression by both mouse and human striatal astrocytes. Mouse striatal astrocytes were FACS-sorted from two distinct models, R6/2 and zQ175 mice, which respectively express exon1-only truncated or full-length HTT, while human astrocytes were generated from either hESCs expressing full-length mHTT, or fetal striatal glia transduced with exon1-only mHTT. Comparison of differential gene expression between each of these conditions and their normal HTT controls, and to one another, revealed astrocyte-specific alterations in both truncated and full-length mHTT models that were shared by both species, yet with differences that clearly distinguished glia derived from each model. Overlap of these data sets revealed that the patterns of mHTT-associated transcriptional dysregulation depended not only upon species, but also upon whether the astroglia expressed truncated or full-length mHTT. These data revealed a common set of conserved, mHTT-associated dysregulated pathways that may present targets for the rescue of glial pathology in HD, while revealing that the gene expression of glia expressing truncated mHTT may differ substantially from that of glia expressing full-length mHTT.
2021-04-07 | GSE154128 | GEO
Project description:Expression data from Bmi1-null common myeloid progenitor (CMP)
| PRJNA144699 | ENA
Project description:Differential hyper- and hypo-methylation regions in G0 versus G4/G5 CMP The goal of this study is to evaluate changes in CpG methylation profilings of telomere dysfunctional common myeloid progenitor cells (CMP) as compared to their wild type controls
2015-04-09 | GSE62392 | GEO
Project description:HOTAIR is a scafold long non-coding RNA tethering PRC2 and Lsd1/REST/coREST complexes to gene promoters to repress transcription of genes involved in epithelial to mesenchymal transition (EMT). To decipher a role of the Lsd1 in HOTAIR function we generated epithelial cell lines expressing full length and truncated versions of HOTAIR missing first 5'-300 (Epi-HOTΔP) and last 3'-500 bp (Epi-HOTΔL) interacting with HOTAIR partners. These cell lines were further used to determine Lsd1 binding sites using chromatin immunoprecipitation approach.
2021-04-22 | GSE106262 | GEO
Project description:The aim of the experiment was to identify accessible (open) chromatin regions in the genome prior to and post induction of EBV's BZLF1 protein. Two versions of BZLF1 were employed: full-length and activation-domain (AD)-truncated BZLF1 non-induced and induced for 15 h. The experiments were performed as triplicates.
2021-02-07 | E-MTAB-8420 | biostudies-arrayexpress