Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA136717 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Targets of Ephrin-A signaling in epidermal keratinocytes
| PRJNA136713 | ENA
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. cSCC cell lines (n=3) were transfected with either control or EphB2 siRNA (75 nM) and incubated for 72 hours. Total RNA was extracted and processed expression profiling with GeneChip 3’ IVT Express Kit according to manufacturer’s protocol.
2015-08-27 | E-GEOD-66361 | biostudies-arrayexpress
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
Project description:Human epidermal keratinocytes were treated with 25 ng.ml EphB2 or EFNA4, both as-Fc conjugates (Sigma). Human epidermal keratinocytes are treated with 25 ng/ml EphB2 or EFNA4 Fc conjugates in a 48hr time course.
2011-03-01 | E-GEOD-26523 | biostudies-arrayexpress
Project description:To gain a global view of the signaling pathways engaged by EphB receptors in the intestinal epithelium, we analyzed the transcriptional alteraltions after acute inhibition of EphB signaling in vivo. An intravenous injection of ephrin-B2-Fc decreases EphB2 tyrosine phosphorylation and results in a reduction in cell proliferation to a similar extent as in EphB2:EphB3 double null mutant mice. Moreover, cells bevome mislocalized along the crypt-villus axis, as in the EphB2;EphB3 --/-- mice, although this is not apparent until several days after injection. By analysing the transcriptome within the first day after blocking EphB signaling, it is possible to study the effect of blocked EphB signaling without the potential secondary effects caused by distorted cell positioning. Since ephrin-B2-Fc binds exclusively to EphB expressing cells inthe crypts in the intestine, it is possible to assess transcriptional alterations in these cells in response to EphB antagonist in whole preparations of colon.
2009-12-18 | E-TABM-753 | biostudies-arrayexpress
Project description:Human epidermal keratinocytes were treated with 25 ng.ml EphB2 or EFNA4, both as-Fc conjugates (Sigma).
2011-03-01 | GSE26523 | GEO
Project description:Transgene line containing the histone gene fused to GFP was established and characterized at genomic, transcriptional and protein level. The GFP tag was then used for ChIP Seq analysis of the DNA sequences bound by H3.2. The analysis revealed interesting ocular specific targets including Ephrin family genes. Altered incorporation of H3.2 was found in the mutant, specifically around the ligand Efna5 and the receptor Ephb2. The effect of this altered incorporation on Ephrin signaling was further analyzed by QPCR and immunohistochemistry. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for GFP (sc-9996)
2022-06-19 | GSE206293 | GEO
Project description:Local cerebral hypoperfusion causes ischemic stroke while driving multiple cell-specific responses including inflammation, glutamate-NMDAR-mediated neurotoxicity, edema formation and angiogenesis. Despite the relevance of these pathophysiological mechanisms for disease progression and outcome, molecular determinants controlling the onset of these processes are only partially understood. In this context, our study intended to investigate the functional role of EphB2 – a receptor tyrosine kinase that is crucial for synapse function and binds to membrane-associated ephrin-B ligands. Cerebral ischemia was induced in EphB2-deficient mice by transient middle cerebral artery occlusion followed by different times (6, 12, 24 and 48 h) of reperfusion. Histological, neurofunctional and transcriptome analyses indicated an increase in EphB2 phosphorylation under these conditions and attenuated progression of stroke in EphB2-deficient mice. Moreover, while infiltration of microglia/macrophages and astrocytes into the peri-infarct region was not altered, expression of the pro-inflammatory mediators MCP-1 or IL-6 was decreased in these mice. In fact, in vitro analyses indicated that binding of EphB2 to astrocytic ephrin-B ligands stimulates NF-κB-mediated cytokine expression via the MAPK pathway. Further magnetic resonance imaging of the EphB2-deficient ischemic brain revealed a lower level of neuronal cytotoxic edema formation within 6 h upon onset of reperfusion. On the mechanistic level, absence of neuronal EphB2 decreased the mitochondrial Ca2+ load upon activation of NMDAR but not AMPAR. Moreover, activation of EphB2 by ephrin-B2 enhanced the NMDA-evoked excitotoxic neuronal cell death in vitro while neuron-specific loss of ephrin-B2 reduced the extent of cerebral tissue damage in the acute phase of ischemic stroke. Collectively, EphB2 may promote the immediate response to an ischemia-reperfusion event in the central nervous system by (i) pro-inflammatory activation of astrocytes via ephrin-B-dependent signalling and (ii) amplification of the NMDA-evoked neuronal excitotoxicity.
2019-02-13 | GSE120565 | GEO
Project description:Objectives: Eph/Ephrin cell-cell signaling is emerging as a key player in tissue fibrogenesis. The aim of this study was to test the hypothesis that the receptor tyrosine kinase EphB2 mediates dermal fibrosis in systemic sclerosis (SSc). Methods: We assessed normal and SSc human skin biopsies for EphB2 expression. The in vivo role of EphB2 in skin fibrosis was investigated by subjecting EphB2-knockout mice to both bleomycin-induced and tight skin (Tsk1/+) genetic mouse models. EphB2 kinase-dead and overactive point mutant mice were used to evaluate the role of EphB2 forward signaling in bleomycin-induced dermal fibrosis. In vitro studies were performed on dermal fibroblasts from SSc patients and healthy controls, which was followed by in vivo analysis of fibroblast-specific EphB2 deficient mice. Results: Expression of EphB2 is upregulated in SSc skin tissue and explanted SSc dermal fibroblasts compared to healthy controls. EphB2 expression is elevated in two animal models of dermal fibrosis. In mice, EphB2 drives dermal fibrosis in both the bleomycin and the Tsk1/+ models of skin fibrosis. EphB2 forward signaling is a critical mediator of dermal fibrosis. Transforming growth factor-β (TGFβ) cytokines upregulate EphB2 in dermal fibroblasts via non-canonical TGFβ/SMAD signaling and silencing EphB2 in dermal fibroblasts is sufficient to dampen TGFβ-induced fibroblast-to-myofibroblast differentiation. Moreover, mice with fibroblast-specific deletion of EphB2 showed impaired fibroblast-to-myofibroblast differentiation and reduced skin fibrosis upon bleomycin challenge. Conclusion: Our data implicate EphB2 overexpression and kinase-mediated forward signaling in the development of dermal fibrosis in SSc. EphB2 thus represents a potential new therapeutic target for SSc.
2024-04-10 | GSE253089 | GEO
Project description:Hypothalamic dysfunction is a key pathological factor in inflammation-associated depression. In the present study, isobaric tags for relative-absolute quantitation (iTRAQ) combined with mass spectrometry were employed to detect the proteomes in the hypothalamus of the lipopolysaccharide (LPS)-induced depression mouse. A total of 187 proteins were differentially expressed compared with the control group. The results indicated altered molecules were clustered into Ephrin receptor signalling; glutamatergic transmission, and inflammation-related signalling. Ephrin type-B receptor 2 (EPHB2), a transmembrane receptor protein in Ephrin receptor signalling, was significantly elevated and interacted with the accumulated NMDAR subunit GluN2A in the hypothalamus. Additionally, molecules involved in synaptic plasticity regulation, such as hypothalamic postsynaptic density protein-95 (PSD-95), p-AKT and brain-derived neurotrophic factor (BDNF), were significantly altered in the LPS-induced depressed group. It might be an underlying pathogenesis that the EPHB2-GluN2A-AKT cascade regulates synaptic plasticity in depression. EPHB2 can be a potential therapeutic target in the correction of glutamatergic transmission dysfunction. In summary, our findings point to the previously undiscovered molecular underpinnings of the pathophysiology in the hypothalamus of inflammation-associated depression and offer potential targets to develop antidepressants.
2020-01-09 | PXD016040 | Pride