Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAsequencing of DOT1L inhibitor EPZ5676 treated ALDH1+ and ALDH1- cell populations

ABSTRACT: Global gene expression profiles obtained after treating cells with DOT1L inhibitor, EPZ5676

ORGANISM(S): Homo sapiens

PROVIDER: GSE194434 | GEO | 2022/01/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNAsequencing of DOT1L inhibitor EPZ5676 treated ALDH1+ and ALDH1- cell populations

Project description:RNAsequencing of DOT1L inhibitor EPZ5676 treated ALDH1+ and ALDH1- cell populations

| PRJNA800650 | ENA

Expression profiling of ethanol-treated and EPZ5676-treated mouse DBA2 SSCs

Project description:We repport the effect of EPZ5676 (DOT1L inhibiotr) on the transcriptome of cultured mouse DBA2 spermatogonial stem cells (SSCs). SSCs were cultured in the presence of 2 uM EPZ5676 or 0.2% ethanol (control) for 2 weeks. We find a number of differentially expressed genes between control and EPZ5676-treated SSCs.

2022-07-26 | GSE181590 | GEO

Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts (ChIP-seq dataset)

Project description:using ChIP-seq we examined Chromatin occupancy of the MLL-fusion complex members Menin and DOT1L after treatment with DOT1L methyltransferase inhibitors EPZ5676 and the novel compounds "compound 10" and "compound 11" as well as with the Menin-inhibitor VTP50469 in MOLM13 cells. Furthermore we used ChiP-seq to quantify the loss of H3K79me2 (histone mark deposited by DOT1L) after treatment with the DOT1L inhibitors EPZ5676 and "compound 10" in MOLM13 and RS4,11 cells.

2020-06-01 | GSE149183 | GEO

Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts (RNA-seq dataset)

Project description:Using 3-end RNA-seq followed by digital gene expression analyses we assessed genes that change expression upon treatment with the DOT1L-methyltransferase inhibitors EPZ5676 and the novel drug "compound 10"

2020-06-01 | GSE149184 | GEO

DOT1L-mediated Murine Neuronal Differentiation associates with H3K79me2 Accumulation and preserves SOX2-Enhancer Accessibility

Project description:To study whether acute inhibition of DOT1L induces global chromatin states alterations, we profile and compare the transcriptome, chromatin accessibility and epigenome (H3K4me3, H3K4me1, H3K27ac, H3K27me3, H3K36me3, H3K9me3, H3K79me2) of mESC and ES-derived NPC, treated with DMSO or EPZ5676.

2020-08-01 | GSE135318 | GEO

Inhibition of DOT1L increases osteoclast fusion and resorption and aggravates bone loss

Project description:Osteoclasts are absorptive cells and play a critical role in homeostatic bone remodeling and pathological bone resorption. Emerging evidence suggests an important role for epigenetic regulation of osteoclastogenesis. In this study, we investigated the role of DOT1L, which regulates gene expression epigenetically by histone H3K79 methylation during osteoclast formation. DOT1L and H3K79me2 levels were upregulated during osteoclast differentiation. Small molecule inhibitor- (EPZ5676 or EPZ004777) or short hairpin RNA-mediated reduction in DOT1L expression promoted osteoclast differentiation and resorption. DOT1L inhibition also increased osteoclast area and accelerated bone mass reduction in a mouse ovariectomy (OVX) model of osteoporosis. DOT1L inhibitors did not alter osteoblast differentiation in vitro and in vivo. Proteomics data, together with bioinformatics analysis, revealed that DOT1L inhibition altered reactive oxygen species (ROS) generation, autophagy activation, and cell fusion-related protein expression. ROS generation increased, and autophagy activation and cell migration ability enhancement were verified subsequently by flow cytometry and transwell migration assays. DOT1L inhibition increased NFATc1 nuclear translocation and NF-κB activation and strengthend osteoclast fusion and expression of resorption-related protein CD9, and MMP9 in osteoclasts derived from RAW264.7. Our findings support a new mechanism of DOT1L-mediated H3K79me2 epigenetic regulation of osteoclast differentiation, implicating DOT1L as a new therapeutic target for osteoclast dysregulation-induced disease.

2018-01-24 | PXD006448 | Pride

Antitumor effects of DOT1L inhibition in retinoblastoma

Project description:Epigenetic dysregulation is one of the molecular mechanisms contributing to retinoblastoma (RB) development. Consistent with this notion, human RB tumors show an aberrant expression of many chromatin regulators whereas normal retina or nontumoral retinal tissues do not have any detectable expression of such proteins. Among the chromatin regulators found to be misregulated in RB, this study focuses on a histone methyltransferase DOT1L to assess the therapeutic potential of its targeting for RB treatment. We found that pharmacological inhibition of DOT1L has growth-inhibitory effects on RB cells by itself and also can sensitize RB cells to standard chemotherapeutic drugs by inducing more robust apoptotic cell death when cells are subjected to combination treatments. To understand the molecular mechanisms underlying the growth inhibition and chemosensitization of RB cells upon DOT1L inhibition, we performed the gene expression profiling in Y79 cells treated with a DOT1L inhibitor EPZ5676 in comparison with a vehicle control by RNA-sequencing to identify differentially expressed genes. Our RNA-seq results revealed that DOT1L inhibition downregulates several genes which are known to be misregulated in cancers, including HMGA2.

2021-12-13 | GSE174167 | GEO

Expression Profiling of Mixed Lineage Leukemia Cells Treated with a Potent Small-Molecule DOT1L Inhibitor

Project description:Cell lines bearing MLL translocations (MV4-11 and MOLM-13) were treated with a potent, selective inhibitor of the DOT1L histone methyl transferase. Treatment of MLL-rearranged cell lines with the DOT1L inhibitor selectively inhibits H3K79 methylation and blocks expression of leukemogenic genes. Here we provide expression profiling data of cells treated with DOT1L inhibitor or vehicle control. MV4-11 cells were treated with 3 uM EPZ004777 (DOT1L inhibitor) or vehicle control (0.1% DMSO) for 2, 4 and 6 days. MOLM-13 cells were treated with 3 uM EPZ004777 (DOT1L inhibitor) or vehicle control (0.1% DMSO) for 6 days. For each unique conditon, 3 biological replicates were generated for expression profiling.

2011-07-11 | E-GEOD-29828 | biostudies-arrayexpress

Gene expression changes upon Dot1L knockdown and Dot1L inhibitor treatment during reprogramming

Project description:Through a loss-of-function approach, we identified that inhibition of the histone methyltransferase, Dot1L, accelerated somatic cell reprogramming, significantly increased the yield of induced pluripotent stem (iPS) cell colonies, and substituted for Klf4 and c-Myc in the reprogramming cocktail. To understand the mechanism by which Dot1L inhibition results in these phenotypes, we carried out gene expression profiling using Affymetrix microarrays. GSM723207-GSM723224: Embryonic stem cell-derived fibroblasts (dH1fs) were retrovirally transduced in culture with vectors expressing either a control shRNA or an shRNA targeting Dot1L. These cells were then superinfected with either Oct4, Sox2, Klf4 and c-Myc (OSKM) retroviruses or Oct4, Sox2 and c-Myc (OSM) retroviruses. Total RNA was harvested 6 days later. There were three biologic replicates for each condition. GSM880675-GSM880682: dH1fs were treated with 10uM Dot1L inhibitor (EPZ004777) and then superinfected with Oct4, Sox2, Klf4 and c-Myc (OSKM) retroviruses. Total RNA was harvested 6 days later. There were two biologic replicates for each condition.

2012-03-01 | E-GEOD-29253 | biostudies-arrayexpress

Profiling of expression data in melanoma cells with mutant DOT1L or treated with DOT1L inhibitor

Project description:DOT1L-dependent H3K79 methylation is associated with telomere silencing, meiotic checkpoint control, DNA repair, modulation of constitutive heterochromatin, and transcriptional activation.

2018-02-14 | GSE103079 | GEO

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