Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-34961E-GEOD-34959
PROVIDER: PRJNA156139 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE34959: Expression profiling of primary wild type (WT), Ezh2-null and Eed-null murine MLL-AF9 AML GSE34961: Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML GSE34962: Epigenetic profiling of WT and Ezh2-null MLL-AF9 murine leukemic cells Refer to individual Series
2012-02-22 | E-GEOD-34963 | biostudies-arrayexpress
Project description:Chromatin immunoprecipitation (ChIP) for H3K27me3 followed by Solexa sequencing in WT and Ezh2-null leukemic cells from primary and secondary recipients. Leukemic cells from primary and secondary recipients of MLL-AF9-transduced WT and Ezh2-null cells were sorted for GFP and YFP expression and analyzed by Chip-Seq.
2012-02-22 | E-GEOD-34962 | biostudies-arrayexpress
Project description:We evaluated gene expression changes in secondary recipient murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of a homozygous conditional allele for Ezh2, a component of the Polycomb Repressive Complex2. For WT cells, 4 biological replicates were hybridized. For Ezh2-null cells, 5 biological replicates were hybridized.
2012-02-22 | E-GEOD-34961 | biostudies-arrayexpress
Project description:Expression profiling of primary wild type (WT), Ezh2-null and Eed-null murine MLL-AF9 AML
| PRJNA156135 | ENA
Project description:Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML
| PRJNA156137 | ENA
Project description:We evaluated gene expression changes in murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of homozygous conditional alleles for Ezh2 or Eed, both of which are components of the Polycomb Repressive Complex2. For WT cells, 3 biological replicates were hybridized. For Ezh2-null cells, 4 biological replicates were hybridized. For Eed-cells, 3 biological replicates were hybridized.
2012-02-22 | E-GEOD-34959 | biostudies-arrayexpress
Project description:Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML
2015-09-22 | E-GEOD-34961 | ExpressionAtlas
Project description:Expression profiling of primary wild type (WT), Ezh2-null and Eed-null murine MLL-AF9 AML
2015-09-22 | E-GEOD-34959 | ExpressionAtlas
Project description:The histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations that involve the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in a murine MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3 and H3K36me3. Histone methylation patterns are highly abnormal on MLL-AF9 fusion target loci, defining a distinct epigenetic lesion involving H3K79. Conditional inactivation of Dot1l leads to specific down-regulation of direct MLL-AF9 targets and an MLL-translocation associated gene expression signature, while global transcription levels remain largely unaffected. This correlated with a greater sensitivity of leukemic blasts towards loss of Dot1l compared to normal hematopoietic cells. Development of in vivo leukemia was absolutely dependent on Dot1l. Chromatin immunoprecipitation followed by Solexa sequencing for H3K4me3, H3K27me3, H3K36me3, H3K79me2 and biotinylated MLL-AF9 in HSC, GMP and LSC.
2011-09-13 | E-GEOD-29130 | biostudies-arrayexpress
Project description:The histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations that involve the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in a murine MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3 and H3K36me3. Histone methylation patterns are highly abnormal on MLL-AF9 fusion target loci, defining a distinct epigenetic lesion involving H3K79. Conditional inactivation of Dot1l leads to specific down-regulation of direct MLL-AF9 targets and an MLL-translocation associated gene expression signature, while global transcription levels remain largely unaffected. This correlated with a greater sensitivity of leukemic blasts towards loss of Dot1l compared to normal hematopoietic cells. Development of in vivo leukemia was absolutely dependent on Dot1l.
2011-09-13 | GSE29130 | GEO