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

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

PROVIDER: PRJEB35064 | ENA |

REPOSITORIES: ENA

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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

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

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

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

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Project description:DNA binding regions of MEF2D transcription factor associated with myogenic regulatory factors were investigated in differentiated myotubes using ChIP-seq analysis.

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Project description:Kasumi-7, Kasumi-9, NAGL-1, and NALM-1 cell lines were subjected to ChIP-seq analysis using anti-H3K27Ac antibody. Input signal reads are also provided.

2020-06-30 | E-MTAB-8463 | biostudies-arrayexpress

GATA-2 occupancy in Kasumi-3 cell line

Project description:GATA-2 is a master regulator of hematopoiesis which controls expression of multiple genes and is implicated in acute myeloid leukemia (AML). However, the molecular mechanism how GATA-2 deregulation causes leukemogenesis is still unclear. In this study, GATA-2 ChIP-squ analysis was conducted in Kasumi-3 AML cell line to identify GATA-2 target genes which play important roles in the pathogenesis of AML. ChIP with GATA-2 antibody was conducted in Kasumi-3 AML cell line and ChIP-seq profile was generated by deep sequencing.

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Next Generation Sequencing of Wild Type and Hnrnpul1-/- RAW 264.7 Cells Transcriptomes

Project description:Purpose: The goal of this study is to compare NGS-derived wild type and Hnrnpul1 knockout (Hnrnpul1-/-) RAW 264.7 cells transcriptomes with or without LPS stimulation. Methods: Sequancing was performed by Novogene China Co. Ltd. RNA profiles of wild type and Hnrnpul1-/- RAW 264.7 cells as well as LPS stimulated (10 h) wild type and Hnrnpul1-/- RAW 264.7 cells were generated by deep sequencing using Illumina Novaseq 6000. Index of the reference genome was built using Hisat2 v2.0.5 and paired-end clean reads were aligned to the reference genome using Hisat2 v2.0.5. featureCounts v1.5.0-p3 was used to count the reads numbers mapped to each gene. And then FPKM of each gene was calculated based on the length of the gene and reads count mapped to this gene. Method of TMM was used to normalize the readcount. Negative binomial distribution model was used to calculate the P value, and FDR was calculated by the method of Benjaminiand Hochberg. Results: Using an optimized data analysis workflow, we mapped about 40 million sequence reads per sample to the mouse genome (GRCm38/mm10). Comparing to wild type RAW 264.7 cells, 237 genes were up-regulated and 181 genes were down-regulated in Hnrnpul1-/- cells. At 10 h following LPS stimulation, 341 genes were up-regulated and 288 genes were down-regulated in Hnrnpul1-/- cells. Genes were pre-ranked according to log2FoldChange(KO/WT) followed by GSEA and 6 gene sets were significantly enriched. Significantly differential genes were undergone GO analysis (biological process) and biological process including cell-cell adhesion, positive regulation of cell activation and regulation of response to external stimulus were enriched. Conclusions: Lacking Hnrnpul1 promotes the expression of inflammatory cytokines in LPS stimulated RAW 264.7 cells.

2022-06-01 | GSE196232 | GEO

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