Figure 7.

A schematic model representing the pathway(s) modulated by HRI that maintains cellular proteostasis. At steady state or upon cellular stress conditions, misfolded proteins are normally targeted for degradation by the ubiquitin-proteosome system (purple line) or lysosomal-dependent autophagy (black line). However, during proteosomal insufficiency induced upon MG132 treatment (in red), HRI-mediated chaperone-assisted selective autophagy (blue lines) that facilitates clearance of p62+/Ub+ as well as p62+/Ub− misfolded proteins (aggresomes) is triggered.