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Analysis of MV4 11 cells treated with ASH1L inhibitor AS-99

ABSTRACT: Analysis of MV4 11 cells treated with ASH1L inhibitor AS-99

PROVIDER: PRJNA631052 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11729915_1.fastq.gz	Fastqsanger.gz
	SRR11729915_2.fastq.gz	Fastqsanger.gz
	SRR11729916_1.fastq.gz	Fastqsanger.gz
	SRR11729916_2.fastq.gz	Fastqsanger.gz
	SRR11729917_1.fastq.gz	Fastqsanger.gz

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Transcriptome of MV4 11 cells treated with ASH1L inhibitor AS-99

Project description:Transcriptome of MV4 11 cells treated with ASH1L inhibitor AS-99

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Aurora-A interactome in MV4-11 cells

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Gene expression changes in MV4-11 cells upon SMARCA4 knock-down and PFI-3 treatment

Project description:Pharmacological inhibition of the SMARCA4 bromodomain inhibited human leukemic cell proliferation, phenocopying SMARCA4 knockdown in these cells. We performed microarray analysis of global gene expression changes in MV4-11 cells after 6 days of PFI-3 treatment and after SMARCA4 knock-down. With this analysis we identified several genes whose expression was similarly up- or down-regulated upon inhibitor treatment and SMARCA4 depletion. Human acute monocytic leukemia cells (MV4-11, ACC 102) were lentivirally transduced with shRNA taregting SMARCA4 (KD) or with a negative control shRNA (Scr). In a parallel experiment MV4-11 cells were treated for 6 days with 10 uM PFI-3, which is SMARCA4, SMARCA2 and PBRM1 bromodomain inhibitor, or DMSO as a negative control. All sample types were prepared in triplicates.

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ASH1L links histone H3 lysine 36 di-methylation to leukemia

Project description:The histone methyltransferases MLL and ASH1L are trithorax-group proteins that interact genetically through undefined molecular mechanisms to regulate developmental and hematopoietic gene expression. Here we show that the lysine 36-dimethyl mark of histone H3 (H3K36me2) written by ASH1L is preferentially bound in vivo by LEDGF, an MLL-associated protein that co-localizes with MLL, ASH1L and H3K36me2 on chromatin genome wide. Furthermore, ASH1L facilitates recruitment of LEDGF and wild type MLL proteins to chromatin at key leukemia target genes, and is a crucial regulator of MLL-dependent transcription and leukemic transformation. Conversely KDM2A, an H3K36me2 demethylase and Polycomb-group silencing protein, antagonizes MLL-associated leukemogenesis. Our studies illuminate the molecular mechanisms underlying epigenetic interactions wherein placement, interpretation and removal of H3K36me2 contribute to the regulation of gene expression and MLL leukemia, and suggest ASH1L as a target for therapeutic intervention. Investigation of multiple transcription factors and histone modification marks in MV4-11 human leukemia cells.

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Genome-wide distribution of ASH1L and H3K36me2 in human MV4 11 leukemia cell line

Project description:Genome-wide distribution of ASH1L and H3K36me2 in human MV4 11 leukemia cell line

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CD36 impacts the expression of genes in MV4-11 cells

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Gene expression changes in MV4-11 cells upon SMARCA4 knock-down and PFI-3 treatment

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