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Mus musculus

ABSTRACT: Gene expression changes upon Mll1 knockout in NUP98-HOXA9 transformed murine LSKs

PROVIDER: PRJNA305926 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2994643_1.fastq.gz	Fastqsanger.gz
	SRR2994643_2.fastq.gz	Fastqsanger.gz
	SRR2994644_1.fastq.gz	Fastqsanger.gz
	SRR2994644_2.fastq.gz	Fastqsanger.gz
	SRR2994645_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Gene expression changes upon Mll1 knockout in NUP98-HOXA9 transformed murine LSKs

Project description:We report Illumina next generation RNA sequencing (RNAseq) of NUP98-HOXA9 in vitro transformed murine LSKs upon genetic deletion of Mll1. These gene expression data illustrate that Mll1 regulates Hoxa, Hoxb and Meis1 expression in NUP98-HOXA9 transformed murine BM cells.

2016-12-11 | GSE75997 | GEO

Genome-wide maps of NUP98 fusion and MLL1 co-bound targets and their chromatin state in NUP98 fusion transformed cells.

Project description:By performing biotin-mediated chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) for two different NUP98 fusions, we defined the genome-wide direct binding sites of NUP98-HOXA9 or NUP98-HOXD13. To test whether NUP98 fusions and Mll1 were recruited to the same region of Hox genes promoters, Mll1 ChIP-seq analysis was carried out in murine NUP98-HOXA9 transformed cells using an anti-Mll1n antibody. In agreement with our results showing that NUP98-HOXA9 interacts with MLL1 in NSL/MLL1 complex, Mll1 binding targets significantly overlap with that of NUP98-HOXA9 at promoter region and gene body region. Given that MOF and MLL1 work in concert to modify H4K16ac and H3K4me3 at promoters, we further test whether H3K4me3 and H4K16ac marks are associated with NUP98-HOXA9-bound targets in murine NUP98-HOXA9 transformed cells by anti-H3K4me3 and anti-H4K16ac ChIP-seq. Our data show that both H3K4me3 and H4K16ac mark presents on NUP98-HOXA9 binding targets at promoters, and this is in line with the coordination role in the activities between MOF-mediated H4K16 acetylation and MLL/SET-mediated H3K4 methylation. In summary, our results confirmed that NUP98-HOXA9 and Mll1 are recruited to the same Hox loci, and this recruitment is associated with activating epigenetic marks, supporting the notion of the association between NUP98 fusions and NSL/Mll1 complex, suggesting that the recruitment of NUP98 fusions to the Hox gene loci maybe through MLL1.

2016-12-11 | GSE76001 | GEO

Genome-wide maps of N_NUP98 and NUP98-TOP1 and MLL1 co-bound targets and their chromatin state in NUP98 fusion transformed cells.

2016-12-21 | GSE83221 | GEO

Mus musculus

Project description:Gene expression changes upon Mof knockout in MLL-AF9 transformed murine LSKs

| PRJNA319638 | ENA

Transcription profiling of mouse bone marrow cells expressing NUP98/HHEX or NUP98/HOXA9 a new oncogenic fusion with acute myeloid leukemia

Project description:We have cloned and characterized a fusion gene NUP98/HHEX1 resulting from t(7;10) from a patient with acute myeloid leukemia (AML). As NUP98/HHEX acts as an aberrant transcriptional activator, putative targets were searched upon transient expression of the fusion in primary murine bone marrow cells. Experiment Overall Design: Murine bone marrow cells were transduced with a retrovirus (MSCV-IRES-GFP, MIG) expressing either NUP98/HHEX or NUP98/HOXA9 (or the empty vector), mRNA was isolated after 72h. Each experiment was performed in triplicates.

2008-06-11 | E-GEOD-10909 | biostudies-arrayexpress

Gene expression profiles upon Meis1 knockout in Hoxa9/Meis1-induced AML

Project description:Meis1 is found cooperatively activated with Hoxa7/a9 in AML, and it indeed promotes leukemogenic activities of Hoxa9. It is important to identify downstream target genes of Meis1 to understand its cooperative activity with Hoxa9 in leukemogenesis. We used microarrays to detail the global programme of gene expression upon Meis1 knockout. Murine primary bone marrow cells of the Rosa26-Cre-ERT2 knock-in mouse were transformed by retroviral transduction of Hoxa9 and floxed Meis1. The immortalized bone marrow cells were treated with 2 μM of 4-hydroxytamoxifen to delete Meis1 cDNA. Gene expression profiles were compared between the original Hoxa9/Meis1-expressing cells and Meis1 deleted (Hoxa9 only) cells.

2015-01-01 | E-GEOD-50645 | biostudies-arrayexpress

Gene expression changes upon Mof knockout in MLL-AF9 transformed murine LSKs

Project description:We report Illumina next generation RNA sequencing (RNAseq) of MLL-AF9 in vitro transformed murine LSKs upon genetic deletion of Mof. These gene expression data illustrate that Mof regulates the expression of genes involved in DNA damage response and chromatin stability in MLL-AF9 transformed cells.

2017-08-30 | GSE80671 | GEO

Trancriptome profiling of murine Hoxa9-transformed MigA9 cell line treated or not with DB818

Project description:Effect of DB818 treatment on murine Hoxa9-transformed MigA9 cell line Effect of DB818 treatment on murine Hoxa9-transformed MigA9 cell line

2021-02-01 | GSE111109 | GEO

Phase Separation by the NUP98-HOXA9 Fusion Oncoprotein Drives an Oncogenic Phenotype in Hematopoietic Cells

Project description:RNA-seq of mouse hematopoietic stem and progenitor cells expressing NUP98-HOXA9 (NHX9) show upregulation of HOX and other NUP98 fusion target genes, but expression changes are dampened or lost with the introduction of mutations in NUP98's FG repeats or HOXA9's DNA binding domain

2021-10-13 | GSE185621 | GEO

MLL is essential for NUP98-HOXA9-induced leukemia

Project description:Rearrangements involving the NUP98 gene resulting in fusions to several partner genes occur in acute myeloid leukemia and myelodysplastic syndromes. This study demonstrates that the second FG repeat domain of the NUP98 moiety of the NUP98-HOXA9 fusion protein is important for its cell immortalization and leukemogenesis activities. We demonstrate that NUP98-HOXA9 interacts with MLL via this FG repeat domain and that, in the absence of MLL, NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. Molecular analyses indicate that MLL is important for the recruitment of NUP98-HOXA9 to the HOXA locus and for NUP98-HOXA9-induced HOXA gene expression. Our data indicate that MLL is crucial for NUP98-HOXA9 leukemia initiation.

2017-02-28 | GSE93923 | GEO

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