Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-cadherin mechanotransduction activates EGFR-ERK signaling in epithelial monolayers by inducing ADAM-mediated ligand shedding

ABSTRACT: E-cadherin mechanotransduction activates EGFR-ERK signaling in epithelial monolayers by inducing ADAM-mediated ligand shedding

PROVIDER: PRJNA1228921 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32500660.fastq.gz	Fastqsanger.gz
	SRR32500661.fastq.gz	Fastqsanger.gz
	SRR32500662.fastq.gz	Fastqsanger.gz
	SRR32500663.fastq.gz	Fastqsanger.gz
	SRR32500664.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

E-cadherin mechanotransduction activates EGFR-ERK signaling in epithelial monolayers by inducing ADAM-mediated ligand shedding

Project description:The behavior of cells is governed by signals originating from their local environment, including mechanical forces that cells experience. Forces are transduced by mechanosensitive proteins, which can impinge on signaling cascades that are also activated by growth factor receptors upon ligand binding. However, the interplay between these mechanical and biochemical signals in the regulation of intracellular signaling networks remains incompletely understood. To elucidate this mechanochemical crosstalk, we conducted phosphoproteomic and transcriptomic analyses on epithelial monolayers subjected to mechanical strain. This approach revealed ERK signaling as a predominant strain-activated hub, initiated at the level of the upstream EGF receptor. Strain-induced EGFR/ERK signaling relies on mechanosensitive E-cadherin adhesions, as this signaling is disrupted upon genetic modulation of force transduction by the E-cadherin complex. Proximity labeling identified a connection between E-cadherin and ADAM17, an enzyme that mediates the shedding of soluble EGFR ligands. We developed a novel ADAM activity probe to demonstrate that mechanical strain induces ADAM activation, which relays mechanosensitive signaling from E-cadherin adhesions towards EGFR/ERK. Collectively, our data demonstrate how mechanical strain transduced by E-cadherin adhesion modulates the presence of EGFR ligands to regulate downstream ERK activity. Our findings illustrate how mechanical signals and biochemical ligands can operate within a single, linear signaling cascade.

2025-05-21 | GSE290599 | GEO

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

Local VE-cadherin mechanotransduction triggers long-ranged remodeling of endothelial monolayers.

Project description:In this study, we present results demonstrating that mechanotransduction by vascular endothelial cadherin (VE-cadherin, also known as CDH5) complexes in endothelial cells triggers local cytoskeletal remodeling, and also activates global signals that alter peripheral intercellular junctions and disrupt cell-cell contacts far from the site of force application. Prior studies have documented the impact of actomyosin contractile forces on adherens junction remodeling, but the role of VE-cadherin in force sensation and its ability to influence endothelial cell and tissue mechanics globally have not been demonstrated. Using mechanical manipulation of VE-cadherin bonds and confocal imaging, we demonstrate VE-cadherin-based mechanotransduction. We then demonstrate that it requires homophilic VE-cadherin ligation, an intact actomyosin cytoskeleton, Rho-associated protein kinase 1 (ROCK1) and phosphoinositide 3-kinase. VE-cadherin-mediated mechanotransduction triggered local actin and vinculin recruitment, as well as global signals that altered focal adhesions and disrupted peripheral intercellular junctions. Confocal imaging revealed that VE-cadherin-specific changes appear to propagate across cell junctions to disrupt distant inter-endothelial junctions. These results demonstrate the central role of VE-cadherin adhesions and the actomyosin cytoskeleton within an integrated, mechanosensitive network that both induces local cytoskeletal remodeling at the site of force application and regulates the global integrity of endothelial tissues.

| S-EPMC4379726 | biostudies-literature

Wool shedding

Project description:Study of natural wool shedding

| PRJEB31930 | ENA

Cadherin-dependent mechanotransduction depends on ligand identity but not affinity.

Project description:This study investigates the relationship between classical cadherin binding affinities and mechanotransduction through cadherin-mediated adhesions. The mechanical properties of cadherin-dependent intercellular junctions are generally attributed to differences in the binding affinities of classical cadherin subtypes that contribute to cohesive energies between cells. However, cell mechanics and mechanotransduction may also regulate intercellular contacts. We used micropipette measurements to quantify the two-dimensional affinities of cadherins at the cell surface, and two complementary mechanical measurements to assess ligand-dependent mechanotransduction through cadherin adhesions. At the cell surface, the classical cadherins investigated in this study form both homophilic and heterophilic bonds with two-dimensional affinities that differ by less than threefold. In contrast, mechanotransduction through cadherin adhesions is strongly ligand dependent such that homophilic, but not heterophilic ligation mediates mechanotransduction, independent of the cadherin binding affinity. These findings suggest that ligand-selective mechanotransduction may supersede differences in cadherin binding affinities in regulating intercellular contacts.

| S-EPMC3516441 | biostudies-literature

Whole genome characterization of in vitro generated mouse colonic monolayers

Project description:We report whole genome data for in vitro mouse monolayers with different culture time/transepithelial electrical resistance and colonic crypts. Mouse colonic monolayers were generated on gradient cross-linked collagen scaffolds.

2019-01-23 | GSE116541 | GEO

Effect of E-cadherin by N-cadherin replacement in mouse intestinal epithelial cells

Project description:We conditionally substituted E-cadherin (E-cad; cadherin 1) with N-cadherin (N-cad; cadherin 2) during intestine development by generating mice in which an Ncad cDNA was knocked into the Ecad locus We used microarray to follow gene expression changes derived from lack of E-cadherin on intestinal epithelial cells

2017-05-01 | GSE81920 | GEO

ADAM17-mediated EGFR ligand shedding directs macrophage-promoted cancer cell invasion

Project description:ADAM17-mediated EGFR ligand shedding directs macrophage-promoted cancer cell invasion

| PRJNA875032 | ENA

Peripheral blood transcriptome responses to Salmonella Typhimurium in pigs differing in Salmonella shedding phenotypes

Project description:Salmonella species infect many vertebrate species, and pigs colonized with Salmonella enterica serovar Typhimurium (ST) are usually asymptomatic, making detection of these Salmonella-carrier pigs difficult. The variable fecal shedding of this gram-negative bacteria in such pigs is an important cause of foodborne illness and zoonotic disease. To investigate gene pathways and biomarkers associated with the variance in Salmonella shedding following experimental inoculation, we have initiated the first analysis of the whole blood transcriptional response induced by Salmonella. A population of pigs (n=40) was inoculated with ST and the peripheral blood and feces were collected between 2 and 20 days post-inoculation. Two groups of pigs with either low shedding (LS) or persistent shedding (PS) phenotypes were identified. The global transcriptional changes in response to ST inoculation were identified by Affymetrix Genechip?analysis of peripheral blood RNA at day 0 and day 2 post-inoculation. Forty pigs (n=40) was inoculated with ST. Four low shedding (LS) pigs and six persistent shedding (PS) pigs were identified. Transcriptom of peripheral blood collected at 0 and 2 dpi were identified by Affymetrix Genechip analysis.

2011-05-28 | E-GEOD-27000 | biostudies-arrayexpress

Transcriptional response of human duodenal enteroid monolayers to norovirus infection

Project description:The goal of this study was to evaluate the transcriptional response of 4 human duodenal enteroid lines on monolayers to norovirus infections (GII.4). Enteroids were plated as monolayers in Intesticult (Stem Cell Technologies) proliferation medium. After 1 day of cell growth as a monolayer, the proliferation medium was changed with differentiation medium for 5 days. Five-day-differentiated monolayers were washed and were either mock-infected or inoculated with human norovirus supplemented with 500 μM glycochenodeoxycholic acid (GCDCA), for 1 to 2 h at 37°C. Total RNA was extracted using the Qiagen RNeasy kit and paired-end Illumina sequencing was performed.

2021-10-01 | GSE183223 | 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