Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: Erk-dependent Epigenetic Reprogramming Underlies Epithelial to Mesenchymal Transition

PROVIDER: PRJNA357255 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5101120.fastq.gz	Fastqsanger.gz
	SRR5101130.fastq.gz	Fastqsanger.gz
	SRR5101140.fastq.gz	Fastqsanger.gz
	SRR5101121.fastq.gz	Fastqsanger.gz
	SRR5101131.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 28

Similar Datasets

Mus musculus

Project description:Genome-scale epigenetic reprogramming during epithelial to mesenchymal transition

| PRJNA143201 | ENA

Erk-dependent Epigenetic Reprogramming Underlies Epithelial to Mesenchymal Transition

Project description:The series of events that allows for the conversion of adherent epithelial cells into migratory cells is collectively known as epithelial-mesenchymal transition (EMT). EMT is involved in triggering neural crest migration during development and in the pathogenesis of diseases, such as cancer metastasis. Whereas Erk signalling is known to be essential for EMT, its influence on the epigenetic and transcriptional programme underlying EMT is poorly understood. Here, using a comprehensive genome-wide analysis of H3K27ac mark and gene expression in primary mammary epithelial cells undergoing EMT, we found that Erk signalling is essential for the epigenetic reprogramming underlying hallmark gene expression and phenotypic changes of EMT. We found that the chemical inhibition of Erk signalling during EMT prevents loss and gain of H3K27ac mark at regulatory regions of epithelial and mesenchymal genes, respectively, and results in a transcriptome and epigenome closer to those of epithelial cells. Further computational analyses identified a distinct set of transcription factor motifs enriched at distal regulatory regions that are epigenetically remodelled by Erk signalling. Altogether, our study reveal an Erk-dependent epigenetic remodelling of distal regulatory elements that results in a gene expression programme that is essential for driving EMT.

2017-06-13 | GSE92333 | GEO

Mus musculus

Project description:Gene expression in epithelial, EMT (epithelial-mesenchymal transition) and MET (mesenchymal-epithelial transition) cells

| PRJNA209196 | ENA

Mus musculus

Project description:Sox4 is a master regulator of epithelial-mesenchymal transition (EMT) by controlling Ezh2 expression and epigenetic reprogramming

| PRJNA194616 | ENA

Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition

Project description:Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition

| PRJNA230687 | ENA

Epigenomic reprogramming during epithelial to mesenchymal transition

Project description:This SuperSeries is composed of the following subset Series: GSE27968: DNA methylation data from AML12 cells during EMT GSE28291: Genome-scale epigenetic reprogramming during epithelial to mesenchymal transition Refer to individual Series

2011-07-03 | E-GEOD-28581 | biostudies-arrayexpress

MS-based quantitative proteomic analysis of ribosomal fractions from wild-type and Zeb1-overexpressing human mammary epithelial cell

Project description:Epithelial-mesenchymal transition (EMT) involves profound changes in cell morphology, driven by transcriptional and epigenetic reprogramming. However, it emerges that translation and the ribosome composition play also key role in establishing physio-pathological phenotypes. Using genome-wide analyses, we report significant rearrangement of the translational landscape and machinery during EMT. Specifically, a mesenchymal cell line overexpressing the EMT transcription factor ZEB1 shows alterations in translational reprogramming and fidelity. Considering the change in translational activity of ZEB1-overexpressing mesenchymal cells, including in fidelity activity, we sought for changes in ribosome composition. We thus performed a riboproteome approach, i.e., mass spectrometry (MS)-based quantitative proteomic analysis of purified cytoplasmic ribosomes to highlight any change in relative amount of individual ribosomal proteins between wild-type and ZEB1-overexpressing human mammary epithelial cells.

2024-11-02 | PXD047409 | Pride

VPA-treatment of Panc-1-cells to study epigenetic impact mediated by histone acetylation on epithelial-mesenchymal transmission

Project description:Non-mesenchymal pancreatic cells are a potential source for cell replacement therapies aiming to restore the endocrine capacity lost during diabetes mellitus. Although a highly complex network of transcription factors underlies the differentiation, growth, and specification of pancreatic precursors, several studies indicated that the transdifferentiation of non-mesenchymal cells can be achieved by epigenetic regulation. The induction of this epithelial-mesenchymal transition through the post-translational modification of histones, exerting control over both dynamic and long-term gene expression, is a promising approach for reprogramming them into mesenchymal cells. The small molecule and histone deacetylase inhibitor valproic acid was linked to the expression of key transcription factors of pancreatic lineage in epithelial cells and insulin transcription. However, the underlying mechanisms are not fully understood. To shed further light on the potential use of valproic acid for cellular reprogramming strategies, we studied its effects on human ductal Panc-1-cells employing next generation RNA sequencing, real-time PCR and protein analysis by ELISA and western blot. Our data indicate a significant regulation of cell cycle, cell adhesion, histone acetyltransferase and metabolism-related genes, and an epithelial–mesenchymal transition through acetylation of histone H3, resulting in the phenotype of a-cells, supporting the prospect of a therapeutic usage of epithelial pancreatic cells for the purpose of reprogramming into hormonesecreting endocrine cells.

2022-02-07 | GSE166640 | GEO

Project description:Epigenomic reprogramming during epithelial to mesenchymal transition

| PRJNA139133 | ENA

Homo sapiens

Project description:Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition [DREAM-seq]

| PRJNA230695 | ENA