Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

H3K79me2 ChIP-seq in prostate cancer cells

ABSTRACT: We report the application of ChIP sequencing technology for high-throughput profiling of H3K79me2 in prostate cancer cells. We generated genome-wide maps of LNCaP and PC3 cells that were treated with the specific DOT1L inhibitor EPZ004777. We find that lysine 79 dimethylation is sensitive to DOT1L inhibition in both cell lines, however the enrichment of K79 methylated peaks differed between the two cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE135574 | GEO | 2019/08/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide maps of chromatin state of H3K79me2 in embryonic and neonatal cardiomyocytes of XMlc2-Cre;Dot1L mutants and controls

Project description:Epigenetic enzymes play critical roles in embryogenesis by defining higher-order chromatin structures required for the establishment of organ-specific transcriptional networks. In this study we investigated the role of the histone 3 lysine 79 methyltrasferase Dot1L in cardiomyocytes during development. We conducted chromatin immunoprecipitation experiments for H3K79me2 in embryonic (E16.5) and neonatal (P1) cardiomyocytes from Dot1L cardiomyocyte-specific conditional knock out and control mice. Genes that bear this modification in DOT1L controls lose it in cKOs, consistent with the model of DOT1L as the sole histone K79 methyltransferase. Overall, we identified enrichment of methylation of H3K79 in gene bodies and in regulatory regions associated wih trascription factors essential for cardiac patterning at E16.5 and with genes important for cardiomyocyte proliferation and maturation in the postnatal period.

2022-11-11 | GSE184109 | GEO

H3K79me2 naïve and in vitro activated B cells

Project description:We studied the role of the histone methyltransferase DOT1L in B cell development and differentiation. H3K79me2 ChIP-sequencing data was generated from sorted B cells. This was compared to RNA-sequencing data from WT and Dot1L KO mice in order to study the link between H3K79me2 and transcription.

2020-11-19 | GSE138906 | GEO

RNA-seq analysis of murine KMT2A-MLLT3 with DOT1L overexpressed

Project description:We transduced two individual murine KMT2A-MLLT3 AML samples with DOT1L and three days after sorting for DOT1L+ cells collected for RNA-seq MLL-rearranged leukemias have been previously shown to be dependent on the presence of histone 3 lysine 79 (H3K79) dimethylation on the genomic targets of the fusion, and an inhibitor of the H3K79 methyltransferase DOT1L is in clinical trials for MLL-rearranged leukemia. In order to ask what biologic effects overexpression of DOT1L would have on the H3K79me2 ChIP-Seq profiles and MLL-fusion target gene expression, murine leukemias generated by transplanting MSCV-MLL-AF9-GFP transduced lin- cKit+ Sca1+ bone marrow cells were subjected to overexpression of DOT1L. Cells were sorted into low (low level of DOT1L overexpression), high (high level of DOT1L overexpression) and bulk (entire population) samples, and subjected to H3K79me2 ChIP-Seq (using a drosophila spike in for normalization) and RNA-Seq analysis 3 days after transduction.

2019-07-10 | GSE134035 | GEO

DOT1L inhibition blocks multiple myeloma cell proliferation through suppressing IRF4-MYC signaling

Project description:Epigenetic alterations play an important role in the pathogenesis in multiple myeloma (MM), but its biological and clinical relevance is not fully understood. Here, we show that DOT1L, which catalyzes methylation of histone H3 lysine 79, is required for the survival of MM cells. Treatment with DOT1L inhibitors induced cell cycle arrest and apoptosis in MM cells, and strongly suppressed cell proliferation in vitro. Chromatin immunoprecipitation-sequencing (ChIP-seq) and microarray analysis revealed that DOT1L inhibition downregulated H3K79 dimethylation (H3K79me2) and expression levels of IRF4-MYC signaling genes in MM cells. Our data suggest that DOT1L may play an essential role in the development of MM, and DOT1L inhibition may provide a new therapy for MM treatment.

2018-09-23 | GSE108661 | GEO

H3K79me2 and H3K4me3 in CD8 T cell subsets

Project description:We studied the role of the histone methyltransferase DOT1L in T cell development and differentiation. H3K79me2 and H3K4me3 ChIP-sequencing data was generated from sorted CD8 single positive thymocytes, naïve CD8 splenocytes and memory CD8 splenocytes. This was compared to RNA-sequencing data from WT and Dot1L KO mice in order to study the link between H3K79me2 and transcription.

2020-07-29 | GSE138908 | GEO

DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (ChIP-seq)

Project description:Enhancer elements are a key regulatory feature of many important genes. Several general features including the presence of specific histone modifications are used to demarcate potentially active enhancers. Here we reveal that putative enhancers marked with H3 lysine 79 (K79) di or trimethylation (me2/3) (which we name H3K79me2/3 enhancer elements or KEEs) can be found in multiple cell types. Mixed lineage leukemia gene (MLL) rearrangements (MLL-r) such as MLL-AF4 are a major cause of incurable acute lymphoblastic leukemias (ALL). Using the DOT1L inhibitor EPZ-5676 in MLL-AF4 leukemia cells, we show that H3K79me2/3 is required for maintaining chromatin accessibility, histone acetylation and transcription factor binding specifically at KEEs but not non-KEE enhancers. We go on to show that H3K79me2/3 is essential for maintaining enhancer-promoter interactions at a subset of KEEs. Together, these data implicate H3K79me2/3 as having a functional role at a subset of active enhancers in MLL-AF4 leukemia cells.

2019-05-30 | GSE117864 | GEO

DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (Capture-C)

2019-05-30 | GSE117863 | GEO

DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (ATAC-seq)

2019-05-30 | GSE117862 | GEO

DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (RNA-seq)

2019-05-30 | GSE128632 | GEO

Expression profiling in Prostate cancer cells treated with DOT1L inhibitor

Project description:We performed expression profiling of prostate cancer cells, LNCaP and PC3 cells that were treated with the specific DOT1L inhibitor EPZ004777 (1uM) for 8 days. We found that unique genes were differentially expressed in both cell lines.

2019-08-09 | GSE135573 | 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