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RNA-seq for gene expression changes upon silencing MEF2D-fusion in a MEF2D-HNRNPUL1 fusion-expressing Kasumi-7 cell line

ABSTRACT: RNA-seq for gene expression changes upon silencing MEF2D-fusion in a MEF2D-HNRNPUL1 fusion-expressing Kasumi-7 cell line

PROVIDER: PRJEB35113 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3624960_1.fastq.gz	Fastqsanger.gz
	ERR3624960_2.fastq.gz	Fastqsanger.gz
	ERR3624961_1.fastq.gz	Fastqsanger.gz
	ERR3624961_2.fastq.gz	Fastqsanger.gz
	ERR3624962_1.fastq.gz	Fastqsanger.gz

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RNA-seq for gene expression changes upon silencing MEF2D-fusion in a MEF2D-HNRNPUL1 fusion-expressing Kasumi-7 cell line

Project description:To explore the mechanisms underlying the maintenance of acute lymphoblastic leukemia harboring fusion genes involving MEF2D transcription factor, the MEF2D-fusion was silenced by shRNA and the resulting gene expression changes were analyzed by RNA-seq.

2020-06-30 | E-MTAB-8480 | biostudies-arrayexpress

MEF2D-HNRNPUL1 ChIP-seq in a genome-edited Kasumi-7 cell line

Project description:Acute lymphoblastic leukemia harboring the fusion genes involving the MEF2D transcription factor (MEF2D-ALL) is associated with poor clinical outcomes. To explore binding sites in the genome in MEF2D-ALL, we genome-edited a MEF2D-ALL cell line Kasumi-7 so that the fusion is tagged with HA at the carboxyl-terminal and co-expressed with GFP. We used this cell line for ChIP-seq using anti-HA antibody. Pair-end reads for Input and HA ChIP DNA are provided.

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ATAC-seq of Kasumi-7 acute lymphoblastic leukemia cell line harboring MEF2D-HNRNPUL1 fusion gene

Project description:ATAC-seq of Kasumi-7 acute lymphoblastic leukemia cell line harboring MEF2D-HNRNPUL1 fusion gene

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MEF2D-HNRNPUL1 ChIP-seq in a genome-edited Kasumi-7 cell line

Project description:MEF2D-HNRNPUL1 ChIP-seq in a genome-edited Kasumi-7 cell line

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ATAC-seq of Kasumi-7 acute lymphoblastic leukemia cell line harboring MEF2D-HNRNPUL1 fusion gene

Project description:ATAC-seq. was performed to examine open chromatin regions in an acute lymphoblastic leukemia cell line, Kasumi-7

2020-06-30 | E-MTAB-8491 | biostudies-arrayexpress

Functional, structural, and molecular characterizations of the leukemogenic driver MEF2D-HNRNPUL1 fusion.

Project description:Recurrent MEF2D fusions with poor prognosis have been identified in B-cell precursor ALL (BCP-ALL). The molecular mechanisms underlying the pathogenic function of MEF2D fusions are poorly understood. Here, we show that MEF2D-HNRNPUL1 (MH) knock-in mice developed a progressive disease from impaired B-cell development at the pre-pro-B stage to pre-leukemia over 10 to 12 months. When cooperating with NRASG12D, MH drove an outbreak of BCP-ALL, with a more aggressive phenotype than the NRASG12D-induced leukemia. RNA-sequencing identified key networks involved in disease mechanisms. In chromatin immunoprecipitation-sequencing experiments, MH acquired increased chromatin-binding ability, mostly through MEF2D-responsive element (MRE) motifs in target genes, compared with wild-type MEF2D. Using X-ray crystallography, the MEF2D-MRE complex was characterized in atomic resolution, whereas disrupting the MH-DNA interaction alleviated the aberrant target gene expression and the B-cell differentiation arrest. The C-terminal moiety (HNRNPUL1 part) of MH was proven to contribute to the fusion protein's trans-regulatory activity, cofactor recruitment, and homodimerization. Furthermore, targeting MH-driven transactivation of the HDAC family by using the histone deacetylase inhibitor panobinostat in combination with chemotherapy improved the overall survival of MH/NRASG12D BCP-ALL mice. Altogether, these results not only highlight MH as an important driver in leukemogenesis but also provoke targeted intervention against BCP-ALL with MEF2D fusions.

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Gene expression signatures of MEF2D-silencing hepatocellular carcinoma cells

Project description:Global expression profiles in Huh7 after infection with Lv-shMEF2D and Lv-scrambled, as well as transfection with siRNA-MEF2D and siRNA-control, were compared to investigate the molecular mechanisms involved in MEF2D-mediated regulation of cell cycle. In order to investigate the molecular mechanisms involved in MEF2D-mediated regulation of cell cycle, we assessed gene expression profiles in Huh7 cells after infection with Lv-shMEF2D and Lv-scrambled, as well as transfection with siRNA-MEF2D and siRNA-control, by cDNA microarray. Analysis of global mRNA expression profile indicated a shift toward G2/M arrest in the cells after downregulating MEF2D expression. The genes that inhibit G2/M transition were found to be expressed in high level in MEF2D-downregulated group, as compared with control group. Meanwhile, mRNA abundance of G2/M transition-promoting genes, except CDC2 and CDC25C, was reduced when MEF2D expression was depressed in Huh7 cells

2015-04-07 | E-GEOD-37123 | biostudies-arrayexpress

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Project description:RNA-seq for gene expression changes upon silencing MEF2D-fusion in a MEF2D-HNRNPUL1 fusion-expressing Kasumi-7 cell line

2020-01-13 | E-MTAB-8480 | ExpressionAtlas

Gene expression signatures of MEF2D-silencing hepatocellular carcinoma cells

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Next Generation Sequencing Quantitative Analysis of Wild Type and AML1-ETO Related Fusion Circular RNA (F-CircAE) Knockdown Kasumi-1 Cells Transcriptomes

Project description:The goal of this study is to determine the difference in transcriptome expression profils between wild type and AML1-ETO related fusion circular RNA knockdown Kasumi-1 cells

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