Figure 2.

Model of prion-like protein aggregate–induced formation of TNTs and intercellular spreading. The aggregation and accumulation of prions or prion-like proteins in an “infected” cell (1) induces an increase in TNT number via an unknown mechanism, e.g., via ROS-induced stress pathways (2). The prion/prion-like aggregates may then be propagated via TNTs from infected cells to naive cells (3), wherein they effect the conversion and seeding of naive self-protein molecules. Adapted from Abounit et al. (2016a).