Fig. 6.

Schematic outline of the regulation of EGFR internalization and mediated signaling by the CIN85–SH3GL2–Cbl complex. a Deletion or inactivation of SH3GL2 (indicated by X) from this complex will allow tumor progression via continuous signaling through the EGFR pathway upon ligand (EGF) stimulation as depicted. b Presence of wild-type SH3GL2 and the appropriately assembled CIN85–SH3GL2– Cbl complex on the other hand will trigger EGFR internalization and subsequent degradation thereby resulting in decreased tumor growth via downregulation of the EGFR signaling pathway