Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide mapping of RNA polymerase active sites in DOT1L-depleted HCT116 cells by PRO-seq analysis

ABSTRACT: Genome-wide mapping of RNA polymerase active sites in DOT1L-depleted HCT116 cells by PRO-seq analysis

PROVIDER: PRJNA1077998 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28007288_1.fastq.gz	Fastqsanger.gz
	SRR28007288_2.fastq.gz	Fastqsanger.gz
	SRR28007289_1.fastq.gz	Fastqsanger.gz
	SRR28007289_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Genome-wide mapping of RNA polymerase active sites in DOT1L-depleted HCT116 cells by PRO-seq analysis

Project description:Precision nuclear run-on sequencing (PRO-seq) approach was adopted to evaluate the effect of DOT1L in regulating transcription and RNA polymerase active sites in HCT116 cells

2024-02-24 | GSE256074 | GEO

PRO-seq from HCT116 cells in normoxia and hypoxia

Project description:PRO-seq analysis was used to examine rapid transcriptional changes in response to short-term hypoxia in WT and HIF1A-/- HCT116 cells

2021-01-29 | GSE145567 | GEO

Raw RNA-seq data from control and Ki-67-depleted HCT116 human colon cancer cells

Project description:Raw RNA-seq data from control and Ki-67-depleted HCT116 human colon cancer cells

2021-07-23 | GSE159160 | GEO

PRO-seq from HCT116 cells in normoxia and hypoxia

Project description:PRO-seq from HCT116 cells in normoxia and hypoxia

| PRJNA607559 | ENA

Common and distinct functions of mouse Dot1l in the regulation of endothelial transcriptome

Project description:Epigenetic mechanisms are mandatory for endothelial cells (ECs) during cardiovascular development. Dot1l-mediated gene transcription in mice is essential for development and function of lymphatic ECs (LECs). The role of Dot1l in development and function of blood ECs (BECs) is unclear. RNA-seq datasets from Dot1l-depleted or -overexpressing BECs and LECs were used to comprehensively analyze regulatory networks of gene transcription and pathways. Dot1l depletion in BECs changed the expression of genes involving cell-to-cell adhesion and immunity-related biological processes. Dot1l overexpression changed the expression of genes involved in different types of cell-to-cell adhesion and angiogenesis-related biological processes. Genes involved in specific tissue development-related biological pathways were altered in Dot1l-depleted BECs and LECs. Vascular endothelial growth factor production-related genes were specifically regulated in BECs by Dot1l. Dot1l overexpression uniquely altered ion transportation-related genes in BECs and immune response regulation-related genes in LECs. Importantly, Dot1l overexpression in BECs led to expression of many genes related to the angiogenesis and mitogen-activated protein kinase signaling pathways. The expression of these genes was unchanged in Dot1l-overexpressing LECs. The findings demonstrate the unique transcriptomic program of ECs and the differential functions of Dot1l in the regulation of gene transcription in BECs and LECs.

2022-10-11 | GSE214945 | GEO

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

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Dot1l ko RNA-seq]

Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector. Results: Inactivation of either Dot1l or Mll1 in this model leads to a substantial delay or complete abrogation of leukemia development. Loss of Dot1l or Mll1 are associated with gene expression changes that have substantial overlap. In addition, genes that are downregulated follwing inactivation of Dot1l or Mll1 have substantial overlap with the gene set upregulated in MN1 transduced CMPs. Conclusions: MN1 mediated leukemogenesis is associated with a gene expression program that dependes on Mll1 and Dot1l Examination of mRNA levels between Dot1l f/f and Dot1l ko, and Mll1 f/f and Mll1 ko.

2016-01-12 | E-GEOD-76748 | biostudies-arrayexpress

Transcriptome analyses by RNA-seq with NELFE knockdown and EPZ-5676 or HMBA treated HCT116 cells

Project description:These analyses aim to investigate transcriptomic changes induced by NELFE knockdown or DOT1L inhibitor (EPZ-5676, 2 uM, 72 h) or p-TEFb activator (HMBA, 10 mM, 24 h) treatment in HCT116 cells

2023-07-01 | GSE234615 | GEO

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

Effect of Dot1l deletion on LSKs and GMPs

Project description:We wanted to investigate the effects of Dot1l deletion on gene expression in LSKs and GMPs of C57/BL6 mice Aberrant Hox gene activation is a recurrent feature in several different types of human leukemia, including leukemias with rearrangements of the mixed lineage leukemia (MLL) gene. In this study, we demonstrate that Hox gene expression is controlled by higher degree H3K79 methylation in acute myeloid leukemia (AML). We show that the deposition of progressive H3K79 methylation states at the genomic loci of critical Hox genes is dependent on the interaction of the H3K79 methyltransferase Dot1l with Af10, a protein that is found in the Dot1l complex isolated from diverse cell types. Furthermore, abrogation of the Dot1l-Af10 interaction reverses aberrant epigenetic profiles found in the leukemia epigenome and impairs the transforming ability of mechanistically distinct AML oncogenes. Lineage negative Sca-1 positive Kit positive (LSK) cells and granulocyte macrophage progenitors (GMPs) were sorted from Dot1 wt/wt x Mx-Cre mice or Dot1l fl/fl x Mx-Cre mice were injected with PIPC. PIPC injection induced biallelic deletion of the Dot1l allele in the Dot1l fl/fl mice but not the Dot1l wt/wt mice. The Dot1l wt/wt LSKs and GMPs were compared to the Dot1l -/- counterparts by RNA extraction and Microarrays.

2014-09-08 | E-GEOD-54498 | 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