Figure 7.

Schemata of proposed pathways. Autophagy promotes cell survival after hyperoxia via interacting with Fas-mediated apoptosis pathways. Hyperoxia induces LC3B expression, a key initiator of autophagy. In this study, we describe dynamic interactions between LC3B and the apoptotic regulator Fas. Forced expression of LC3B was found to diminish apoptotic pathway initiation by the Fas-dependent death-inducing signaling complex. The interactions of LC3B and Fas are dependent on caveolin-1 and its phosphorylation state at Y-14. The balance between LC3B/cav-1/Fas complex determines the fate of the cell.