Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Fosl2 overexpression and Ezh2 inhibition in mouse embryonic fibroblasts

ABSTRACT: Fosl2 overexpression and Ezh2 inhibition in mouse embryonic fibroblasts

PROVIDER: PRJNA900535 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22262229_1.fastq.gz	Fastqsanger.gz
	SRR22262229_2.fastq.gz	Fastqsanger.gz
	SRR22262230_1.fastq.gz	Fastqsanger.gz
	SRR22262230_2.fastq.gz	Fastqsanger.gz
	SRR22262231_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 30

Similar Datasets

Fosl2 overexpression and Ezh2 inhibition in mouse embryonic fibroblasts

Project description:To assess the impact of AP-1 chromatin remodelling, we over-expressed one AP-1 family member, namely Fra2 (encoded by Fosl2), in mouse embryonic fibroblasts (MEFs). To assess the impact of general chromatin depression, we inhibited the activity of PRC2 component histone-lysine N-methyltransferase Ezh2 in MEFS.

2024-07-15 | GSE217780 | GEO

Affinify Purification of EZH2 and phosphodeficient EZH2 identifies phosphorylation dependent interactions of EZH2

Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.

2018-07-03 | PXD010073 | Pride

Mapping interactome networks of FOSL1 and FOSL2 in human Th17 cells

Project description:The differentiation of Th17 cells is controlled by a complex network of transcription factors (TFs), including FOS and JUN proteins of the AP-1 family. The FOS-like proteins, FOSL1 and FOSL2 have recently been reported to control Th17 responses. The molecular mechanisms dictating their roles, however, are unclear. Moreover, although the functions of AP-1 TFs are largely governed by their protein-protein interactions, these are also poorly characterized in this milieu. Using affinity purification in combination with mass-spectrometry we established the first interactomes of FOSL1 and FOSL2 in human Th17 cells. In addition to their known interactions with JUN proteins, our analysis identified several novel binding partners of FOSL factors. Gene ontology analysis revealed RNA binding was enriched as the major functionality for FOSL1 and FOSL2 associated proteins, thereby suggesting possible mechanistic links that have not been studied before. Intriguingly, 29 interactors were found to be shared between FOSL1 and FOSL2, which included crucial regulators of Th17-fate. These findings, including unique and shared interactions, were validated using parallel reaction monitoring targeted mass-spectrometry (PRM-MS), with additional measurements with other laboratory methods. Overall, this study provides key insights into interaction-based signalling mechanisms of FOSL1 and FOSL2, which potentially control Th17 cell-development and associated pathologies.

2021-11-02 | PXD025729 | Pride

Validation of EZH2 targets in GSCs treated with shNT (control), shMELK, shFOXM1, and EZH2 overexpression

Project description:We demonstrate that the catalytic subunit of Polycomb Repressive Complex 2, EZH2, is targeted by the MELK-FOXM1 complex, which in turn promotes resistance to radiation in GSCs. Clinically, EZH2 and MELK are co-expressed in GBM and significantly induced in post-irradiation recurrent tumors whose expression inversely correlated with patient prognosis. Through gain-and loss-of-function study, our data show that MELK or FOXM1 contributes on GSC radioresistance by regulation of EZH2. We used microarrays to validate EZH2 target gene expression. GSCs were treated with shNT (control), shMELK, shFOXM1, and EZH2 overexpression. Total RNA was isolated using the Qiagen RNeasy kit (Qiagen).

2015-04-16 | E-GEOD-63963 | biostudies-arrayexpress

Overexpression of circCUL2 in normal fibroblasts

Project description:Overexpression of circCUL2 in normal fibroblasts

| PRJNA722732 | ENA

Effect of HOXB13 overexpression on osteogenic differentiation in mouse embryonic fibroblasts (MEFs)

Project description:Studies of the effect of HOXB13 overexpression on mesenchymal stem cell (MSC) marker expression and osteogenic differentiation in mouse embryonic fibroblasts (MEFs)

2020-02-25 | GSE145813 | GEO

EZH2 Inhibition as a Therapeutic Strategy for Lymphoma with EZH2 Activating Mutations

Project description:This SuperSeries is composed of the following subset Series: GSE40970: ChIP-seq analysis of H3K27me3 histone modification in EZH2 mutant and wild type DLBCL cell lines GSE40971: Gene expression profiling of EZH2 mutant and wild type DLBCL cell lines treated with EZH2 inhibitor GSE41239: Gene expression profiling of two DLBCL cell lines upon shRNA mediated knockdown of EZH2 Refer to individual Series

2012-10-12 | E-GEOD-40972 | biostudies-arrayexpress

The transcription factor Fosl2 controls systemic autoimmunity by repressing FoxP3 during T cell development

Project description:Purpose: We aimed to charaterise the transfriptional effects of Fosl2 in T cells Methods: We used wt, Fosl2 overexpressing (Fosl2tg) and Fosl2 knock-out (Fosl2ko) CD4+ naive T cells that we stimulated for 24 hours with anti-CD3 and anti-CD28. RNA-was extracted and sequenced using Results: We identified a set of genes whose expression is regulated by Fosl2 in T cells, including Foxp3.

2020-09-04 | GSE132313 | GEO

human prostate and breast epithelial cell lines under EZH2 adenovirus overexpression

Project description:Transcriptional profiling of human prostate and breast epithelial cells with a time course analysis of EZH2 overexpression of cells at 3, 6, 12, 24, 48, and 72 hrs respectively. Keywords: Genetic modification

2007-11-01 | GSE8144 | GEO

EZH2 inhibition induces HLA class I re-expression in Merkel Cell Carcinoma

Project description:We hypothesized that EZH2 could be involved in immune escape in Merkel Cell Carcinoma (MCC). In this context, we aimed at evaluating whether EZH2 might contribute to HLA-I expression repression in MCC. To this purpose, we first investigated whether low/lack of HLA-I expression is associated with high H3K27me3 levels in MCC tumor samples. Whole proteome analysis of the PeTa cell line by mass spectrometry after DZNeP treatment (EZH2 inhibitor) revealed upregulation of proteins involved in Fc receptor, as well as antigen processing and presentation pathways components.

2023-11-21 | PXD040973 | 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