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Mus musculus

ABSTRACT: Genome wide mapping of histone 3 lysine 79 dimethylation in MLL-AF6 murine leukemias

PROVIDER: PRJNA184352 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR638997.fastq.gz	Fastqsanger.gz
	SRR638998.fastq.gz	Fastqsanger.gz
	SRR638999.fastq.gz	Fastqsanger.gz

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Genome wide mapping of histone 3 lysine 79 dimethylation in MLL-AF6 murine leukemias

Project description:We report the genome wide distribution of H3K79 dimethylation in mouse MLL-AF6 positive leukemias to assess whether this epigenetic mark drives MLL-target gene expression. Examination of H3K79 dimethylation in bone marrow cells from sacrificed terminally ill MLL-AF6 positive leukemic mice. The retroviral MSCV-IRES-neo-MLL-AF6 construct was transduced into mouse bone marrow lineage negative Kit +, Sca + (LSK) cells and these cells were injected after G418 selection into irradiated syngenic mice to establish MLL-AF6 positive leukemias.

2013-04-03 | E-GEOD-43062 | biostudies-arrayexpress

Genome-wide analysis of H3K79 methylation in CD34+ CD19+ cells from normal marrow, MLL-rearranged or MLL-germline ALL

Project description:We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). ChIP-chip analysis demonstrated increased histone H3 Lysine 79 (H3K79) dimethylation that correlated with Mll-AF4 associated gene expression profiles in murine ALLs, and in human MLL-rearranged leukemias. In addition, human MLL-rearranged ALLs can be distinguished from other ALLs by their genome-wide H3K79 methylation profiles. Keywords: Cell type comparison

2008-11-04 | GSE12360 | GEO

Genome-wide analysis of H3K79 dimethylation in MLL-AF4 leukemic bone marrow

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Genome-wide analysis of H3K79 dimethylation in normal and MLL-AF4 leukemic pre-B cells

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Genome wide mapping of histone 3 lysine 79 dimethylation in MLL-AF6 murine leukemias

Project description:We report the genome wide distribution of H3K79 dimethylation in mouse MLL-AF6 positive leukemias to assess whether this epigenetic mark drives MLL-target gene expression.

2013-04-03 | GSE43062 | GEO

Expression data from a human MLL-AF6 positive AML cell line

Project description:The MLL gene on chromosome 11 fuses to the AF6 gene on chromosome 6 in a balanced chromosomal translocation that is characetristic of certain adult and pediatric human leukemias. We established a murine leukemia model of MLL-AF6 using the retroviral MLL-AF6 contruct in a bone marrow transplantation system. The ML2 human MLL-AF6 positive leukemia cell line was used for gene expression profiling to assess the transctiptional profile in MLL-AF6 leukemias.

2013-04-03 | GSE43068 | GEO

Expression data from a human MLL-AF6 positive AML cell line

2013-04-03 | E-GEOD-43068 | biostudies-arrayexpress

Expression data from MLL-AF6 positive leukemia cells

2013-04-03 | GSE43067 | GEO

Genome wide mapping of histone 3 lysine 79 dimethylation in MLL rearranged and control human leukemia cell lines

Project description:We report the genome wide distribution of H3K79 dimethylation in the human MLL-AF6 rearranged cell line ML2 as well as the human MOLM13 and HL60 cell lines Examination of H3K79 dimethylation in the MLL-AF6 fusion positive human leukemia cell line ML2 and control cell lines MOLM-13 and HL60. The MLL-AF6 positive ML2 cell line (obtained from DSMZ) and the cell lines HL60 and MOLM 13 were grown under standard conditions and 1 million cells were fixed/crosslinked and used for ChIP-seq with H3K79 dimethylation specific antibody Ab3594 (Abcam)

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RNA-seq analysis of murine KMT2A-MLLT3 with DOT1L overexpressed

Project description:We transduced two individual murine KMT2A-MLLT3 AML samples with DOT1L and three days after sorting for DOT1L+ cells collected for RNA-seq MLL-rearranged leukemias have been previously shown to be dependent on the presence of histone 3 lysine 79 (H3K79) dimethylation on the genomic targets of the fusion, and an inhibitor of the H3K79 methyltransferase DOT1L is in clinical trials for MLL-rearranged leukemia. In order to ask what biologic effects overexpression of DOT1L would have on the H3K79me2 ChIP-Seq profiles and MLL-fusion target gene expression, murine leukemias generated by transplanting MSCV-MLL-AF9-GFP transduced lin- cKit+ Sca1+ bone marrow cells were subjected to overexpression of DOT1L. Cells were sorted into low (low level of DOT1L overexpression), high (high level of DOT1L overexpression) and bulk (entire population) samples, and subjected to H3K79me2 ChIP-Seq (using a drosophila spike in for normalization) and RNA-Seq analysis 3 days after transduction.

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