Fig. 9.

Model illustrating translational regulation of β-catenin by BBR: (A) In the absence of BBR, an active mTORC1 pathway phosphorylates and inactivates 4E-BP1, thus releasing eIF4E from 4E-BP1. MNKs then phosphorylate and activate eIF4E. eIF4E interacts with other components of the translational machinery to form eIF4F, which is recruited to 5′-mRNA cap to initiate cap-dependent translation of β-catenin. This leads to increased cell survival. (B) BBR inactivates mTORC1, leading to dephosphorylation and activation of 4E-BP1 and its interaction with eIF4E. BBR also inhibits MNK-induced eIF4E phosphorylation. This leads to disassembly of eIF4F and repression of β-catenin translation. Repression of β-catenin sensitizes the cells toward increased cell death.