EphrinB2/EphB4-mediated regulation of cytoskeletal contractility is a key homeostatic mechanism of lymphatic endothelial cell-cell junction maintenance, and provides a potential target for therapeutic modulation of lymphatic vessel permeability and function.
EphrinB2 promotes glioblastoma stem-like cell malignancy through the interplay of cell-autonomous and non-cell-autonomous mechanisms and its targeting suppresses tumourigenesis in preclinical models of human glioblastoma.
Notch ligands Jag1 and Dll4 and their effector Ephb2 are required in sinus venosus endocardium for primitive coronary vasculature formation and later for arterial differentiation and maturation of coronary endothelium.
Eph receptor signaling commonly excludes migrating embryonic cells from regions of high ligand density; however, in sea urchin embryos pigmented immunocytes are attracted to regions expressing high levels of Ephrin.
Competition between neurons for postsynaptic ephrin-B3 controls distribution of a limited pool of synapses and defines a novel trans-synaptic mechanism enabling neurons to set the number of synapses they receive.
The internalization of the angiogenic receptor VEGFR2 expressed in neurons is controlled by ephrinB2 and is required for neuronal dendritic arborization, spine morphogenesis and circuitry development in the hippocampus.