Figure 7 | Cell Death & Disease

Figure 7

From: Celastrol targets proteostasis and acts synergistically with a heat-shock protein 90 inhibitor to kill human glioblastoma cells

Figure 7

Celastrol causes proteotoxicity via a thiol-sensitive mechanism in human glioblastoma. Poly-ubiquitinated protein aggregates along with the autophagy substrate and stress sensor, p62, accumulate as a result of defective protein degradation quality-control mechanisms, namely autophagy and proteasomal degradation. The disruption in proteostasis is further substantiated by the activation of cytoprotective heat-shock responses (HSP72/90)

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