Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (RNA-seq)

ABSTRACT: Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (RNA-seq)

PROVIDER: PRJNA820052 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18489131.fastq.gz	Fastqsanger.gz
	SRR18489132.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (ChIP-seq)

Project description:This study characterized the genome-wide binding of histone 3 lysine 79 tri-methylation and expression profile of DOT1L knockdown in OVCAR5 cells.

2022-11-08 | GSE199473 | GEO

Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (RNA-seq)

Project description:This study characterized the genome-wide binding of histone 3 lysine 79 tri-methylation and expression profile of DOT1L knockdown in OVCAR5 cells.

2022-11-08 | GSE199472 | GEO

Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells

Project description:Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells

| PRJNA820049 | ENA

Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (ChIP-seq)

Project description:Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (ChIP-seq)

| PRJNA820051 | ENA

Heightened DOT1L-AF10 enriches H3K79me3 to promote pro-atherogenic inflammatory endothelial phenotype through NF-κB p65

Project description:DOT1L-catalyzed H3K79 methylation is a hallmark of actively transcribed genes and has been extensively studied in developmental and disease contexts. While DOT1L inhibition has emerged as a promising therapeutic strategy in cancer, its role in pro-atherogenic endothelial inflammation remains unclear. To investigate this, we utilized an in vivo partial carotid artery ligation model and observed increased DOT1L expression and H3K79me3 level. Consistently, in vitro studies employing a 3D-printed human coronary artery model and TNF-α stimulation corroborated these results, showing elevated DOT1L expression and H3K79me3 deposition, while levels of H3K79me and me2 remained unchanged. Further analyses identified key DotCom complex components, AF10 and AF9 (upregulated) and AF17 (downregulated), as contributors to the enhanced H3K79me3 landscape. CUT&RUN sequencing showed prominent H3K79me3 enrichment at the RELA (NF-κB p65) promoter, corresponding with increased NF-κB p65 expression and activation. Notably, inhibition/knockdown of the methyltransferase DOT1L or overexpression of the demethylase FBXL10 significantly reduced H3K79me3 levels, thereby suppressing NF-κB p65 expression and attenuating endothelial inflammation, independent of canonical NF-κB p65 activation. These findings establish DOT1L-mediated H3K79me3 as a crucial epigenetic regulator of endothelial inflammation, highlighting a potential therapeutic avenue for mitigating NF-κB p65-driven pro-atherogenic endothelial dysfunction.

2025-12-16 | GSE295366 | GEO

Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-08 | GSE199474 | GEO

Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells (RNA-seq)

Project description:This study characterized the genome-wide binding of FOXK2 in ovarian cancer (OC) cell OVCAR-5 and investigated the expression profile of OVCAR5 cells with FOXK2 knocking-down.

2022-05-18 | GSE173779 | GEO

Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells (ChIP-seq)

Project description:This study characterized the genome-wide binding of FOXK2 in ovarian cancer (OC) cell OVCAR-5 and investigated the expression profile of OVCAR5 cells with FOXK2 knocking-down.

2022-05-18 | GSE173777 | GEO

Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells

Project description:Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells

| PRJNA726996 | ENA

DOT1L regulates pericentromeric heterochromatin

Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.

2023-05-26 | PXD028824 | Pride

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