In the SOD1^G93A mouse model of amyotrophic lateral sclerosis (ALS), expression of transmembrane signaling molecule ephrinB2 in spinal cord astrocytes contributes to motor neuron damage and loss of diaphragm function.

Boundary cell identity and sharpening of borders are coupled in hindbrain development since both are regulated by mechanical tension.

The Netrin-1 and ephrin-B2 proteins act synergistically in the developing nervous system.

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.

Extracellular signals mediated by the EphB2 receptor tyrosine kinase may access the effectors of fundamental cell functions controlled by MYCBP2.

EphA signaling plays dual opposite roles on axon dynamics in neurons, so it inhibits and promotes axon growth through ligand binding and receptor processing, respectively.

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.

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.

A distinctive novel mechanism of ephrin-A/EphA signaling modulation in retinal growth cones ensures concurrent quantitative accuracy and adaptability of topographic hardwiring.

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.