Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CHIP-seq in WT, p53-ko, Ezh2-ko primary macrophages

ABSTRACT: CHIP-seq in WT, p53-ko, Ezh2-ko primary macrophages

PROVIDER: PRJNA754017 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15423420_1.fastq.gz	Fastqsanger.gz
	SRR15423420_2.fastq.gz	Fastqsanger.gz
	SRR15423421_1.fastq.gz	Fastqsanger.gz
	SRR15423421_2.fastq.gz	Fastqsanger.gz
	SRR15423422_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

ATAC-seq in WT, p53-ko, Ezh2-ko primary macrophages

Project description:Assess chromatin accessibility in WT, p53-ko, Ezh2-ko primary macrophages using ATAC-seq.

2022-05-11 | GSE181943 | GEO

ATAC-seq in WT, p53-ko, Ezh2-ko primary macrophages

Project description:ATAC-seq in WT, p53-ko, Ezh2-ko primary macrophages

| PRJNA754018 | ENA

CHIP-seq in WT, p53-ko, Ezh2-ko primary macrophages

Project description:We immunoprecipitated chromatin in primary macrophages using antibodies against Ezh2, p53, H3K27ac, H3K27me3 and Sirt1 to identify the potential binding genes.

2022-05-11 | GSE181942 | GEO

CHIP-seq and ATAC-seq in WT, p53-ko, Ezh2-ko primary macrophages

Project description:CHIP-seq and ATAC-seq in WT, p53-ko, Ezh2-ko primary macrophages

| PRJNA754014 | ENA

Full proteome analysis of WT and Ezh2-KO K562 cells

Project description:Chemotherapy resistance is the main impediment in the treatment of acute myeloid leukaemia (AML). Despite rapid advances, the various mechanisms that lead to resistance development remain to be defined in detail. Here we report that loss-of-function mutations (LOF) in the histone methyltransferase EZH2 have the potential to confer resistance against the chemotherapeutic agent cytarabine. We identify seven distinct EZH2 mutations leading to loss of H3K27 trimethylation via multiple mechanisms. Analysis of matched diagnosis and relapse samples reveal a heterogenous regulation of EZH2 and a loss of EZH2 in 50% of patients. We confirm that loss of EZH2 induces resistance against cytarabine in the cell lines HEK293T and K562 as well as in a patient-derived xenograft (PDX) model. Proteomics and transcriptomics analysis reveal that resistance is conferred by upregulation of multiple direct and indirect EZH2 target genes that are involved in apoptosis evasion, augmentation of proliferation and alteration of transmembrane transporter function. Our data indicates, that loss of EZH2 results in upregulation of its target genes, providing the cell with a selective growth advantage, which mediates chemotherapy resistance.

2021-03-12 | PXD023139 | Pride

The regulatory roles of Ezh2 in response to lipopolysaccharide (LPS) in macrophages and mice with conditional Ezh2 deletion with LysM-Cre system

Project description:The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. With a single LPS stimulation, Ezh2 null(Ezh2flox/flox; LysM-Crecre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2fl/fl; LysM-Cre−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3.

2023-07-20 | PXD041265 | Pride

CHIP-seq and ATAC-seq in WT, p53-ko, Ezh2-ko primary macrophages

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

2022-05-11 | GSE181944 | GEO

Expression data from PPARg WT and KO macrophages

Project description:PPARg is a nuclear receptor that plays an important role in lipid metabolism, homeostasis and immunity. Microarray analysis of gene expression was performed in macrophages from WT and PPARg KO mice. Differentially expressed genes were selected for further analysis. RNA from WT and PPARg KO macrophages was purified for hybridization on Affymetrix microarrays. Peritoneal macrophages were harvest from WT and PPARg KO mice 3 days after intraperitoneal injection of 2.5ml of 3% thioglycollate.

2010-09-24 | E-GEOD-24292 | biostudies-arrayexpress

ATAC-seq analysis in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

Project description:ATAC-seq analysis in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

| PRJNA545887 | ENA

Bone marrow derived macrophages RNA-Seq (WT vs SIRPa KO)

Project description:RNA transcriptome difference between WT and SIRPa knockout (KO) bone marrow derived macrophages (BMDMs). To understand how SIRPa inhibits the phagocytotic capacity of macrophages, a mouse lacking SIRPa was generated, and the transcriptional profiles of BMDMs from wild-type and SIRPa KO mice were compared, using RNA sequencing.

2023-10-02 | GSE223059 | 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