Fig. (5).

A dimer model for Ras-mediated effector activation. (Left) GTP-loaded Ras can each recruit an effector molecule onto the membrane, but the event alone does not activate the effector. The effector is activated when two Ras-GTP molecules form a dimer to also bring two effector molecules into a dimer, which in turn initiates oncogenic signaling. Multiple factors, including membrane binding through the lipid-modified HVR, scaffold proteins, and direct G-domain contacts, could contribute to the dimer formation and hence oncogenic activity of Ras; (Right) Mechanisms that disrupt Ras dimer formation would also inhibit Ras-mediated oncogenesis and therefore could be exploited for anti-cancer therapy.