Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Small molecule-induced epigenomic reprogramming of APL blasts leading to antiviral-like response and c-MYC downregulation [RNA-seq]

ABSTRACT: The epigenomic effects of maltonis, a novel maltol-derived molecule with promising antiproliferative activity against leukemic cells, have been characterized in the APL NB4 cell line. We demonstrate that maltonis treatments induce a profound remodulation of the histone code, reducing global H3K9me3 signal and modulating other histone post-translational modifications (HPTMs). Transcriptomic and epigenomic analyses revealed that maltonis exposure of NB4 cells induces changes in the expression of hundreds of genes (551 upregulated and 288 downregulated) in association with the modulation of the permissive HPTMs histone H3 lysine 4 trimethylation (H3K4me3) and histone H3 lysine 27 acetylation (H3K27ac) at their gene promoters. The upregulation of interferon alpha and gamma and the downregulation of c-MYC target genes have been identified as most significant pathways modulated by maltonis. Most importantly, c-MYC is strongly downregulated by maltonis and represents the common denominator of the downregulated gene sets, suggesting a central role of this gene in the biological response of NB4 cells to maltonis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE205345 | GEO | 2022/12/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Small molecule-induced epigenomic reprogramming of APL blasts leading to antiviral-like response and c-MYC downregulation [ChIP-seq]

Project description:The epigenomic effects of maltonis, a novel maltol-derived molecule with promising antiproliferative activity against leukemic cells, have been characterized in the APL NB4 cell line. We demonstrate that maltonis treatments induce a profound remodulation of the histone code, reducing global H3K9me3 signal and modulating other histone post-translational modifications (HPTMs). Transcriptomic and epigenomic analyses revealed that maltonis exposure of NB4 cells induces changes in the expression of hundreds of genes (551 upregulated and 288 downregulated) in association with the modulation of the permissive HPTMs histone H3 lysine 4 trimethylation (H3K4me3) and histone H3 lysine 27 acetylation (H3K27ac) at their gene promoters. The upregulation of interferon alpha and gamma and the downregulation of c-MYC target genes have been identified as most significant pathways modulated by maltonis. Most importantly, c-MYC is strongly downregulated by maltonis and represents the common denominator of the downregulated gene sets, suggesting a central role of this gene in the biological response of NB4 cells to maltonis.

2022-12-15 | GSE205344 | GEO

Enhancer Mapping in Chronic Lymphocytic Leukemia

Project description:<p>In this study we profile the epigenomic enhancer landscapes of CLL B cells (CD19+/CD5+) harvested from peripheral blood of patients from our Center. Included are results of ChIPseq profiling using chromatin immunoprecipitation of the enhancer histone mark H3K27ac (acetylated lysine 27 on histone H3), and open chromatin profiles using ATAC-seq (assay for transposase accessible chromatin). These profiles are used to define the global enhancer and super enhancer landscape of CLL B cells, and to derive active transcription factor networks associated with this disease. Also included are H3K27ac ChIP-seq and ATAC-seq datasets for non-CLL B cells obtained from the peripheral blood of normal adult donors.</p>

| phs001704 | dbGaP

A critical density of histone H3 lysine 9 tri-methylation is required for propagation of heterochromatin and epigenetic inheritance

Project description:Occupancy profiling of myc-tagged Raf1 protein in fission yeast. Occupancy profiling of lysine 9 dimethylated and trimethylated histone H3 in fission yeast.

2021-06-09 | GSE162701 | GEO

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming

Project description:This SuperSeries is composed of the following subset Series: GSE29146: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [ChIP] GSE29147: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi] GSE29148: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO] GSE29150: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [Transduction] Refer to individual Series

2011-11-29 | E-GEOD-29305 | biostudies-arrayexpress

TOR targets a nuclear RNA processing network to support cell proliferation and control developmental gene expression [ChIP-chip]

Project description:Occupancy profiling of lysine 9 dimethylated histone H3 in fission yeast. Occupancy profiling of MYC-tagged or GFP-tagged Pir1 protein in fission yeast. Occupancy profiling of FLAG-tagged Rec12-DNA linkages during meiosis of fission yeast.

2020-12-22 | GSE142486 | GEO

Cell-Type Specific Profiling of Histone Post-Translational Modifications in the Adult Mouse Striatum

Project description:Histone post-translational modifications (hPTMs) regulate gene expression via changes in chromatin accessibility and transcription factor recruitment. At a given locus, the coordinated enrichment of several distinct hPTMs regulate gene expression in response to external stimuli. However, neuronal hPTMs have been primarily characterized in bulk brain tissue and/or tissue pooled across subjects. This obscures both cell-type and individual variability, features essential to understand individual susceptibility to psychiatric disease. To address this limitation, we optimized a hybrid protocol, ICuRuS, to profile both activating and repressive hPTMs in a single neuronal subtype from a single mouse. We report here profiling of striatal medium spiny neuron (MSN) subtypes, genetically defined by expression of Adenosine 2a Receptor (A2a) or Dopamine Receptor D1 (D1), which differentially regulate reward processing and pathophysiology. Using ICuRuS, we defined genome-wide, A2a- or D1-specific combinatorial hPTM profiles, and discovered regulatory epigenomic features at genes implicated in neurobiological function and disease.

2022-11-17 | GSE193673 | GEO

miRNA genes in HMEC and HMF

Project description:This SuperSeries is composed of the following subset Series: GSE28374: DNA methylation of miRNA genes in HMEC and HMF GSE28375: Histone H3 acetylation of miRNA genes in HMEC and HMF GSE28376: Histone H3 lysine 27 trimethylation of miRNA genes in HMEC and HMF GSE28377: Histone H3 lysine 4 trimethylation of miRNA genes in HMEC and HMF GSE28378: Histone H3 lysine 9 dimethylation of miRNA genes in HMEC and HMF Refer to individual Series

2011-04-05 | E-GEOD-28380 | biostudies-arrayexpress

Impaired transcriptional profile in the hippocampus following loss of Kdm5a

Project description:KDM5A encodes a histone lysine demethylase that removes methyl groups from lysine 4 of histone H3, resulting in repression of target genes. In order to identify KDM5A targets, we profiled transcripts from hippocampi of WT and Kdm5a -/- mice. Loss of KDM5A resulted in dysregulation of 450 genes (FDR-corrected P ≤0.05 and log2 fold change ≥|0.3|), of which 191 genes were upregulated and 259 genes were downregulated.

2020-12-14 | GSE147435 | GEO

Dimethyl alpha-ketoglutarate inhibits proliferation in diffuse intrinsic pontine glioma by reprogramming epigenetic and transcriptional networks

Project description:Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive pediatric brain tumor with limited therapeutic options. Here, we investigated the potential of dimethyl alpha-ketoglutarate (DMKG) as an anti-proliferative agent against DIPG and unraveled its underlying molecular mechanisms. DMKG exhibited robust inhibition of DIPG cell proliferation, colony formation, and neurosphere growth. Transcriptomic analysis revealed substantial alterations in gene expression, with upregulated genes enriched in hypoxia-related pathways and downregulated genes associated with cell division and the mitotic cell cycle. Notably, DMKG induced G1/S phase cell cycle arrest and downregulated histone H3 lysine 27 acetylation (H3K27ac) without affecting H3 methylation levels. The inhibition of AKT and ERK signaling pathways by DMKG coincided with decreased expression of the CBP/p300 coactivator. Importantly, we identified the c-MYC-p300/ATF1-p300 axis as a key mediator of DMKG's effects, demonstrating reduced binding to target gene promoters and decreased H3K27ac levels. Depletion of c-MYC or ATF1 effectively inhibited DIPG cell growth. These findings highlight the potent anti-proliferative properties of DMKG, its impact on epigenetic modifications, and the involvement of the c-MYC-p300/ATF1-p300 axis in DIPG, shedding light on potential therapeutic strategies for this devastating disease.

2023-10-26 | GSE237008 | GEO

Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response

Project description:This SuperSeries is composed of the following subset Series: GSE22102: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (sequencing) GSE24774: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient DCs) GSE24776: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient MEFs) Refer to individual Series

2012-03-02 | E-GEOD-24826 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data