Figures & data
Figure 1. Schematic of the proposed pathways. Hyperoxia increases cellular reactive oxygen species (ROS) production which promotes the expression and activation of LC3B, through a pathway dependent on c-Jun-NH2-terminal kinase (JNK). We describe dynamic interactions between LC3B and the apoptotic regulator Fas. The interactions of LC3B and Fas depend on phospho-caveolin-1. LC3B provides transient cytoprotection against hyperoxia by sequestering Fas. This association precludes formation of the death-inducing signaling complex (DISC), which consists of Fas, Fas-associated death domain protein (FADD) and caspase-8. The balance between LC3B-cav-1-Fas complex formation determines cell fate.
