Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differential expression of genes upon E-cadherin loss of function

ABSTRACT: Differential expression of genes upon E-cadherin loss of function

PROVIDER: PRJNA980087 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24826100_1.fastq.gz	Fastqsanger.gz
	SRR24826100_2.fastq.gz	Fastqsanger.gz
	SRR24826101_1.fastq.gz	Fastqsanger.gz
	SRR24826101_2.fastq.gz	Fastqsanger.gz
	SRR24826102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Differential expression of genes upon E-cadherin loss of function

Project description:In this work by growing monolayers upto 70-80% confluency we study the differential expression of genes upon E-cadherin loss of function

2024-11-14 | GSE234079 | GEO

Differential regulation of proteins upon E-cadherin loss of function

Project description:In this project we undertook mass spectometry to measure differential expression of proteins using MDCK Wild Type (control) against MDCK E-cadherin Knock out

2025-07-14 | PXD043091 | Pride

Differential Notch target genes expression profile upon HDAC3 loss-of-function.

Project description:Differential Notch target genes expression profile upon HDAC3 loss-of-function.

| PRJNA416379 | ENA

RNAi profiling of human mammary epithelial cells - analysis of the effects of loss of E-cadherin and cell adhesion

Project description:Loss of the epithelial adhesion molecule E-cadherin is thought to enable metastasis by disrupting intercellular contactsâan early step in metastatic dissemination. To further investigate the molecular basis of this notion, we use two methods to inhibit E-cadherin function that distinguish between E-cadherinâs cell-cell adhesion and intracellular signaling functions. While the disruption of cell-cell contacts alone does not enable metastasis, the loss of E-cadherin protein does, through induction of an epithelial-to-mesenchymal transition, invasiveness and anoikis-resistance. We find the E-cadherin binding partner ï¢-catenin to be necessary but not sufficient for induction of these phenotypes. In addition, gene expression analysis shows that E-cadherin loss results in the induction of multiple transcription factors, at least one of which, Twist, is necessary for E-cadherin loss-induced metastasis. These findings indicate that E-cadherin loss in tumors contributes to metastatic dissemination by inducing wide-ranging transcriptional and functional changes. Experiment Overall Design: Gene expression changes induced by knockdown of E-cadherin, expression of dominant-negative E-cadherin and double knockdown of E-cadherin and Beta-catenin in immortalized human mammary epithelial cells Experiment Overall Design: Four groups, three biological replicates per group. shCntrl expressing cells are the control group

2008-11-06 | E-GEOD-9691 | biostudies-arrayexpress

Analysis of the effects of loss of E-cadherin and cell adhesion on human mammary epithelial cells

Project description:Loss of the epithelial adhesion molecule E-cadherin is thought to enable metastasis by disrupting intercellular contacts - an early step in metastatic dissemination. To further investigate the molecular basis of this notion, we use two methods to inhibit E-cadherin function that distinguish between E-cadherin's cell-cell adhesion and intracellular signaling functions. While the disruption of cell-cell contacts alone does not enable metastasis, the loss of E-cadherin protein does, through induction of an epithelial-to-mesenchymal transition, invasiveness and anoikis-resistance. We find the E-cadherin binding partner beta-catenin to be necessary but not sufficient for induction of these phenotypes. In addition, gene expression analysis shows that E-cadherin loss results in the induction of multiple transcription factors, at least one of which, Twist, is necessary for E-cadherin loss-induced metastasis. These findings indicate that E-cadherin loss in tumors contributes to metastatic dissemination by inducing wide-ranging transcriptional and functional changes. Keywords: E-cadherin knockdown, dominant-negative E-cadherin expression, E-cadherin and Beta-catenin double knockdown

2008-01-15 | GSE9691 | GEO

Differential Notch target genes expression profile upon HDAC3 loss-of-function.

Project description:The Notch signaling pathway regulates several differentiation and developmental processes in both pre- and post-natal life and its aberrant regulation leads to diseases, including cancer. Here, we investigated the role of histone deacetylase 3 (HDAC3) on the regulation of the Notch-dependent gene expression program in mouse pre-T (Beko) cells. We first defined Notch target genes as those genes that are downregulated upon inhibition of the Notch pathway using DAPT, a gamma-secretase inhibitor (GSI). Subsequently, we investigated the role of HDAC3 in the regulation of Notch target genes by shRNA- and pharmacologically (apicidin)-mediated loss-of-function of HDAC3.

2020-02-04 | GSE106361 | GEO

Differential squamous cell fates elicited by NRF2 gain-of-function versus KEAP1 loss-of-function

Project description:Differential squamous cell fates elicited by NRF2 gain-of-function versus KEAP1 loss-of-function

| PRJNA1077254 | ENA

Amyloid peptide β-dependent loss of endothelial barrier function

Project description:Alzheimer’s disease is the most common form of dementia and is associated with the accumulation of amyloid peptide β in the brain parenchyma. Vascular damage and microvascular thrombosis contribute to the neuronal degeneration and the loss of brain function typical of this disease. In this study, we utilised a murine model of Alzheimer’s disease to evaluate the neurovascular effects of this disease. Upon detection of an increase in the phosphorylation of the endothelial surface receptor VE-cadherin, we focused our attention on endothelial cells.

2022-05-19 | PXD030300 | Pride

Esophageal keratinocyte invasion after loss of E-cadherin and TGF receptor type II

Project description:Esophageal cancer is one of the deadliest cancers as patients present at late stages of disease. Frequent gene alterations include the loss of E-cadherin and TGFb receptor type II. The goal of this study was to establish a model of esophageal cancer by introducing dominant-negative mutants of E-cadherin and TGFb receptor II. To analyze the functional consequences and gene expression chages induced by E-cadherin and TGFb receptor type II loss in esophageal cancer. Human esophageal keratinocytes were retrovirally transfected with wild-type full length E-cadherin, dominant-negative E-cadherin and dominant-negative TGFb receptor type II. Grown in organotypic cultures on a collagen/matrigel matrix with embedded fibroblast, the generated cell lines were analyzed for their potential to invade into the underlying matrix. Each cell lines was grown in duplicate in organotypic culture and therefore 2 replicates analyzed. Gene expression changes in invasive versus non-invasive areas were analyzed after RNA isolation using laser-capture microdissection resulting in 2 samples representing a normal esophageal epithelium (Ecad), 2 each of dominant-negative Ecad (Ecyto) non-invasive and invasive. To model the genetic alterations in esophageal cancer dominant-negative E-cadherin and dominant-negative TGFb receptor type II (Ecyto-dnTGFR) were expressed and 2 samples each, non-invasive and invasive, analyzed.

2013-11-12 | E-GEOD-19472 | biostudies-arrayexpress

Esophageal keratinocyte invasion after loss of E-cadherin and TGF receptor type II

2013-11-12 | GSE19472 | GEO