Skip to main content
. Author manuscript; available in PMC: 2010 Jul 7.
Published in final edited form as: Cancer Cell. 2009 Jul 7;16(1):9–20. doi: 10.1016/j.ccr.2009.04.009

Figure 7. A model depicting ligand-dependent inhibition and ligand-independent stimulation of cell migration and invasion by EphA2.

Figure 7

A. In the absence of ligand, EphA2 is a substrate of Akt activated in tumor cells due to growth factor receptor activation or loss of PTEN. EphA2 phosphorylated on S897 promotes cell polarization, lamellipodium protrusion and cell migration. S897A mutant of EphA2 is sufficient to block chemotactic cell migration.

B. Ephrin-A1 stimulation causes tyrosine phosphorylation in the juxtamembrane domain and serine dephosphorylation on S897 of EphA2, which prevents lamellipodium protrusion and inhibits cell migration.