Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cell-specific information processing in segregating populations of Eph receptor-ephrin-expressing cells

ABSTRACT: Cell-specific information processing in segregating populations of Eph receptor-ephrin-expressing cells

INSTRUMENT(S): LTQ Orbitrap, instrument model

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell

SUBMITTER: Claus Jorgensen

PROVIDER: PRD000814 | Pride | 2009-12-11

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	PRIDE_Exp_Complete_Ac_10295.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_10295.pride.mztab.gz	Mztab
	PRIDE_Exp_Complete_Ac_10295.xml.gz	Xml
	PRIDE_Exp_Complete_Ac_10296.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_10296.pride.mztab.gz	Mztab

Items per page:

1 - 5 of 6

Publications

Cell-specific information processing in segregating populations of Eph receptor ephrin-expressing cells.

Jørgensen Claus C Sherman Andrew A Chen Ginny I GI Pasculescu Adrian A Poliakov Alexei A Hsiung Marilyn M Larsen Brett B Wilkinson David G DG Linding Rune R Pawson Tony T

Science (New York, N.Y.) 20091201 5959

Cells have self-organizing properties that control their behavior in complex tissues. Contact between cells expressing either B-type Eph receptors or their transmembrane ephrin ligands initiates bidirectional signals that regulate cell positioning. However, simultaneously investigating how information is processed in two interacting cell types remains a challenge. We implemented a proteomic strategy to systematically determine cell-specific signaling networks underlying EphB2- and ephrin-B1-cont ...[more]

PMID: 20007894

Similar Datasets

Genome-wide analysis of changes in gene expression induced by Eph and ephrin stimulation of mouse neural progenitors

Project description:The hypothesis tested in the present study was that activation of Eph or ephrin signaling in neural progenitors induces a transcriptional response which participate in the control of progenitor self-renewal. Results provide important information on transcriptional changes in response to activation of Eph receptors. They also show that activation of ephrin signaling does not induce a transcriptional response at genome-wide level.

2017-09-21 | GSE104068 | GEO

Analysis of the gene expression profile in cutaneous squamous cell carcinoma cells after EphB2 knockdown

Project description:The role of Eph/ephrin signaling in numerous biological processes has been established. However, Eph/ephrin signaling has been shown to have complex role in tumor progression. The role of EphB2 receptor in the progression of cutaneous squamous cell carcinoma (cSCC) has not been studied before. EphB2 is significantly overexpressed in cSCC cells compared with normal human epidermal keratinocytes (NHEKs). We used microarray based global gene expression profiling to study the effect of EphB2 knockdown on the expression of different genes in cSCC cells.

2015-08-27 | GSE66361 | GEO

Analysis of the gene expression profile in cutaneous squamous cell carcinoma cells after EphB2 knockdown

2015-08-27 | E-GEOD-66361 | biostudies-arrayexpress

Single methyl group positioning opens new chemical space for EPH receptor kinase inhibition

Project description:EPHrin receptors (EPH) are transmembrane receptor tyrosine kinases. Their extracellular domains bind specifically to ephrin A/B ligands, and this binding modulates the intracellular kinase activity. EPHs are key players in bidirectional intercellular signalling, controlling cell morphology, adhesion and migration. They are increasingly recognized as cancer drug targets. We analysed the binding of the patented Novartis inhibitor NVP-BHG712 (NVP) to EPHA2 and EPHB4. Unexpectedly, all tested commercially available NVP samples were regioisomers NVPiso with a single methyl group binding to an adjacent nitrogen atom compared to the patented compound. The two compounds of identical mass reveal different binding modes. Further, both, in vitro and in vivo experiments show that the isomers differ in their kinase affinity and selectivity.

2018-09-05 | PXD009188 | Pride

Identification of immediate early transcriptional targets of ephrin-B1 forward signaling

Project description:The goal of this study was to identify immediate early transcriptional targets of ephrin-B1 forward signaling that are relevant to palatogenesis. The Ephs compose a family of receptor tyrosine kinase signaling molecules that can be activated by their cognate ligands, the ephrins. Despite the importance of Eph/ephrin signaling in a wide variety of developmental and cell biological processes, a potential downstream transcriptional response has not been explored. To understand the role of ephrin-B1 signaling in palatogenesis, we examined transcriptional response to ephrin-B1 in a primary mouse embryonic palatal shelf cell culture system. We find an immediate early signature of gene expression that reflects the activation of Erk/MAPK signaling by ephrin-B1 signaling in the palatal shelves. Induction of primary palate cells with 2 ug/ml of pre-clustered ephrin-B1 for one hour. Uninduced primary palate cells are the control. Four replicates each.

2010-09-20 | E-GEOD-23539 | biostudies-arrayexpress

Ubiquitin ligase and signalling hub MYCBP2 is required for efficient EPHB2 tyrosine kinase receptor function

Project description:Eph receptor tyrosine kinases participate in a variety of normal and pathogenic processes during development and throughout adulthood. This versatility is likely facilitated by the ability of Eph receptors to signal through diverse cellular signalling pathways: primarily by controlling cytoskeletal dynamics, but also by regulating cellular growth, proliferation, and survival. Despite many proteins linked to these signalling pathways interacting with Eph receptors, the specific mechanisms behind such links and their coordination remain to be elucidated. In a proteomics screen for novel EPHB2 multi-effector proteins, we identified human MYC binding protein 2 (MYCBP2 or PAM or Phr1). MYCBP2 is a large signalling hub involved in diverse processes such as neuronal connectivity, synaptic growth, cell division, neuronal survival, and protein ubiquitination. Our biochemical experiments demonstrate that the formation of a complex containing EPHB2 and MYCBP2 is facilitated by FBXO45, a protein known to select substrates for MYCBP2 ubiquitin ligase activity. Formation of the MYCBP2-EPHB2 complex does not require EPHB2 tyrosine kinase activity and is destabilised by binding of ephrin-B ligands, suggesting that the MYCBP2-EPHB2 association is a prelude to EPHB2 signalling. Paradoxically, the loss of MYCBP2 results in increased ubiquitination of EPHB2 and a decrease of its protein levels suggesting that MYCBP2 stabilises EPHB2. Commensurate with this effect, our cellular experiments reveal that MYCBP2 is essential for efficient EPHB2 signalling responses in cell lines and primary neurons. Finally, our genetic studies in C. elegans provide in vivo evidence that the ephrin receptor VAB-1 displays genetic interactions with known MYCBP2 binding proteins. Together, our results align with the similarity of neurodevelopmental phenotypes caused by MYCBP2 and EPHB2 loss of function, and couple EPHB2 to a signalling effector that controls diverse cellular functions.

2024-01-29 | PXD041786 | Pride

Identification of immediate early transcriptional targets of ephrin-B1 forward signaling

2010-09-21 | GSE23539 | GEO

Effect of EphrinB2 on gene expression in cultured lymphatic endothelial cells (LECs) under hypoxia

Project description:EphrinB2 (erythropoietin-producing hepatoma interactor B2) is a key member of the Eph/ephrin family, promoting angiogenesis, vasculogenesis, and lymphangiogenesis during embryonic development. However, the role of EphrinB2 in cardiac lymphangiogenesis following myocardial infarction (MI) and the potential molecular mechanism remains to be demonstrated.

2024-10-11 | GSE279328 | GEO

Eph-ephrin signaling couples endothelial cell sorting and arterial specification

Project description:Eph-ephrin signaling couples endothelial cell sorting and arterial specification

| PRJNA928081 | ENA

The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells

Project description:Background: Arrhythmogenic cardiomyopathy (ACM) is a genetic autosomal disease characterized by abnormal cell-cell adhesion, cardiomyocyte death, progressive fibro-adipose replacement of the myocardium, arrhythmias and sudden death. Several different cell types contribute to the pathogenesis of ACM, including, as recently described, cardiac stromal cells (CStCs). In the present study, we aim to identify ACM-specific expression profiles of human CStCs derived from endomyocardial biopsies of ACM patients and healthy individuals employing TaqMan Low Density Arrays for miRNA expression profiling, and high throughput sequencing for gene expression quantification. Results: We identified 5 miRNAs and 272 genes as significantly differentially expressed. Both the differentially expressed genes as well as the target genes of the ACM-specific miRNAs were found to be enriched in cell adhesion related biological processes. Functional similarity and protein interaction based network analyses performed on the identified deregulated genes, miRNA targets and known ACM-causative genes revealed clusters of highly related genes involved in cell adhesion, extracellular matrix organization, lipid transport and ephrin receptor signaling. Conclusions: We determined for the first time the coding and non-coding transcriptome characteristic of ACM cardiac stromal cells, finding evidence for a potential contribution of miRNAs to ACM pathogenesis or phenotype maintenance. Besides known pathways, we identified also deregulation of genes encoding ephrin receptors and ephrins, thus suggesting a potential involvement of Eph-ephrin signaling in CStCs from ACM hearts.

2018-06-27 | GSE95120 | 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