Background
R-Ras, a member of the small GTPase family, is homologous to H-, K- and N-Ras, but does not activate MAP kinase pathways and is only weakly oncogenic. Instead, R-Ras is engaged in integrin activation. The effector loop and the carboxy-terminal proline-rich and prenylation sites of R-Ras are critical for integrin activation. Phosphorylation by EphB2 receptor tyrosine kinase and Src at Tyr66 of R-Ras suppresses integrin activity.
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