Morphological profiling of untreated HCT116 cells using Cell Painting reveals a signature of bortezomib resistance, providing a proof-of-concept for the unbiased analysis of drug resistance.

The simultaneous monitoring of transcription, translational control, protein production and proteolysis in the same system can improve our understanding of how cancer cells respond to chemotherapy.

Reducing the expression of 19S subunits shifts the ratio of 20S/26S proteasome complexes and provides a powerful survival advantage in the face of lethal proteasome inhibition.

A new unfolded protein response has been discovered that is distinct from the heat shock response and protects mammalian cells from proteotoxic stress.

Peptidase activity of DDI2 is required to activate Nrf1 in order to enable proteasome recovery in response to proteasome inhibition.

In response to proteotoxic stress, squamous cell carcinoma cells hijack the integrated stress response to promote recovery by bolstering protection of microtubule dynamics.

The nodes of the cytosolic proteostasis network can control sensitivity to proteasome inhibitors and decreased levels of the 19S proteasomal regulator can lead to increased resistance to inhibitors.

Post-translational processing of the SKN-1A/Nrf1 transcription factor regulates proteasome expression.

A common genomic deletion in various human cancers disrupts mitochondrial protein homeostasis in a way that might be targeted by existing drugs.

Myostatin signaling governs neonatal longitudinal muscle growth and neuromuscular contractures in a sex-dependent manner, identifying a potential avenue for contracture treatment and underscoring the need to consider sex as a biological variable in the pathophysiology of acquired neuromuscular disorders.