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.

A new Cereblon-recruiting bifunctional tau ligand, QC-01-175, promotes aberrant tau degradation and rescue of stress vulnerability in human neuronal cell models of tauopathy.

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.

Anticancer compound library screen identified many types of nucleolar stress and revealed an essential role of transcriptional cyclin-dependent kinases in nucleolar structure and function.

Deep learning combined with induced pluripotent stem cell technology is an effective method to interrogate cellular phenotypes and predict patterns of cardiotoxicity in vitro.

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

The proteasomal deubiquitinase UCHL5/UCH37 uses a face distinct from the canonical ubiquitin binding site to engage K48-linked ubiquitin chains and catalyze chain debranching.

Divergence in immunoproteasome substrate specificity and regulation from the constitutive proteasome impacts peptide cleavage quantity and the cellular capacity of the ubiquitin-proteasome system.

Genetic and biochemical approaches reveal that mammalian cells possess a novel DDI2 and transcription-independent pathway for the rapid recovery of proteasome activity after clinically relevant pulse treatment with proteasome inhibitors.

The inhibitory or deletion effect of MELK does not impair the proliferation of basal-like breast cancer cell lines.