E-cadherin promotes EPHA2– ephrin-A1 localization at epithelial cell junctions
EPHA2 is upregulated in many cancers and its expression has been linked to increased malignancy and a poor clinical prognosis.
EPHA2 seems to be preferentially expressed in malignant breast and prostate cancers with a basal phenotype.
EPHA1 is downregulated in advanced human skin and colorectal cancers, EphB receptors are downregulated in advanced colorectal cancer and ephrin-A5 is downregulated in glioblastomas
TNF-alpha, VEGFA and HIF2A upregulate ephrin-A1 in cultured endothelial cells.
Endothelial ephrin-B2 is upregulated by VEGF through the Notch pathway.
“Forward�? signaling corresponds to the proto- typical RTK mode of signaling, which is triggered by ligand binding and involves activation of the kinase domain.
However, the activation mechanisms of Eph receptors have unique features as compared to other RTK families.
Binding between Eph receptors and ephrins on juxtaposed cell surfaces leads to oligomerization through not only Eph receptor – ephrin interfaces but also receptor – receptor cis interfaces located in multiple domains
Phosphorylation of the conserved tyrosine in the activation loop appears to be less critical for Eph receptor activation than it is for many other RTKs, although it may be important for maximal activity.
Participates in complexes:
In compartment: Cytoplasm
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