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. 2014 Apr 1;111(15):E1481–E1490. doi: 10.1073/pnas.1321811111

Fig. 6.

Fig. 6.

Model depicts chaperone competition between protein aggregates and the CME pathway. (A) Under normal conditions, HSC70 is at sufficiently high levels to mediate CME, as well as basal protein client folding. (B) Under disease conditions, where protein aggregates have accumulated and cytosolic HSC70 levels have been titrated, CME is inhibited, but this inhibition can be restored by increasing chaperone levels.