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RNA-seq profiling of mouse embryonic fibroblasts treated with WM-2474 or DMSO

ABSTRACT: RNA-seq profiling of mouse embryonic fibroblasts treated with WM-2474 or DMSO

PROVIDER: PRJNA473346 | ENA |

REPOSITORIES: ENA

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RNA-seq profiling of mouse embryonic fibroblasts treated with WM-2474 or DMSO

Project description:Acetylation of histones by lysine acetyltransferases (KATs) is essential for chromatin organization and function. The MYST family of KATs (KAT5-8) includes the oncogenes KAT6A (MOZ) and KAT6B (MORF/QKF). KAT6A has essential roles in normal hematopoietic stem cells and is the target of recurrent chromosomal translocations, causing acute myeloid leukemia. Similarly, chromosomal translocations in KAT6B have been identified in diverse cancers. KAT6A suppresses cellular senescence via regulation of suppressors of the CDKN2A locus, a function that requires its KAT activity. Loss of one allele of KAT6A extends the median survival of mice with MYC-induced lymphoma from 105 to 413 days. These findings suggest that inhibition of KAT6A and KAT6B may provide a therapeutic benefit in cancer. We have produced a series of highly potent, selective inhibitors of KAT6A/B including WM-8014 and WM-1119, which we anticipate will be useul in accelerating development of therapeutics. For comparison purposes, we also generated an inactive analogue WM-2474 as a control treatment. The data here focus on WM-2474 and present RNA-seq profiling of mouse embryonic fibroblasts (MEFs) treated with either WM-2472 or DMSO.

2018-08-03 | GSE114963 | GEO

RNA-seq profiling of mouse embyonic fibroblasts treated with the Myst inhibitor WM-8014

Project description:Acetylation of histones by lysine acetyltransferases (KATs) is essential for transcriptional regulation of gene expression. The MYST family of KATs (KAT5-8) includes the oncogenes KAT6A (MOZ) and KAT6B (MORF/QKF). KAT6A has key roles in promoting cell proliferation through transcriptional activation of negative regulators of the Cdkn2a locus, which encode the tumor suppressors INK4A and ARF. We produced a series of highly potent, selective inhibitors of KAT6A/B including WM-8014 and WM-1119. Biochemical and structural studies demonstrate that these compounds are reversible acetyl-CoA competitors. WM-8014 and WM-1119 inhibit MYST-catalyzed histone acetylation, thereby inducing cell cycle exit and cellular senescence, without causing DNA damage. The data here examine the transcriptional effects of WM-8014. Mouse embryonic fibroblasts (MEFs) were treated with either WM-8014 or with WM-2474, an inactive control, for either 96 hours or 240 hours and RNA-seq profiling was undertaken.

2018-08-03 | GSE108243 | GEO

Epigenetic profiling of cells following WM-1119 treatment

Project description:ChIP-seq analysis of MOLM-13 human leukemia cells treated with DMSO or WM-1119 for 4 days

2021-10-20 | GSE157042 | GEO

Transcriptional profiling of cells following WM-1119 treatment

Project description:RNA-seq analysis of MOLM-13 human leukemia cells or mouse ER-Hoxa9 treated with DMSO or WM-1119 for 4 days

2021-10-20 | GSE156947 | GEO

Metabolomics Workbench ST000003 - GNPS - Metabolomic analysis of mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells

Project description:mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells were compared via metabolomic analysis

2018-08-02 | MSV000082680 | GNPS

Transcriptomic analysis of DMSO treatment on mouse embryonic fibroblasts (MEFs) during cardiac transdifferentiation

Project description:Cardiac transdifferentiation represents an attractive way of reversing heart damage caused by myocardial infarction. Yet, it is still in pre-clinical stage mainly due to the lack of efficacy with current transdifferentiation protocols. Here, we describe that dimethyl sulfoxide (DMSO) is capable of augmenting cardiomyocyte transdifferentiation in vitro. Treatment of Gata4, Hand2, Mef2c and Tbx5 (GHMT) - transduced mouse embryonic fibroblasts (MEFs) with 1% DMSO induced ~5 fold increase in the percentage of Myh6-mCherry+ cells, and significantly increased the global expression of cardiac genes. Transcriptomic studies were carried out to explore the underlying mechanism of how DMSO may enhance cardiac transdifferentiation.

2020-03-02 | GSE146154 | GEO

RNA-seq profiling of mouse embyonic fibroblasts treated with the Myst inhibitor WM-8014

Project description:RNA-seq profiling of mouse embyonic fibroblasts treated with the Myst inhibitor WM-8014

| PRJNA422909 | ENA

Metabolomic analysis of mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells

Project description:mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells were compared via metabolomic analysis

2013-01-16 | ST000003 | MetabolomicsWorkbench

Mycena sp. WM isolate:WM

Project description:Mycena sp. WM isolate:WM Genome sequencing

| PRJNA725593 | ENA

Gene expression profiling of mouse embryonic kidney (E12.5) treated with CHIR99021 or DMSO

Project description:Purpose: To investigate GSK3 inhibitor effect on gene expression during renal development. Methods: mRNA profiles of in-vitro organ culture of mouse embryonic kidney (E12.5) treated with 5 µM CHIR99021 or 0.1% DMSO for 72 hours were generated by deep sequencing in quadruplicate. Results: When comparing CHIR99021 group to DMSO group, in 30890 genes tested, 950 genes were upregulated, and 1,879 genes were downregulated, with a fold change ≥2 and p (padj value) <0.05.

2021-05-01 | GSE131240 | GEO

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