The McsB kinase is critical for protein quality control in Gram-positive bacteria, assembling a gated phosphorylation chamber during heat-shock conditions to selectively mark misfolded proteins for degradation.
UBIAD1 mediates a unique geranylgeranyl pyrophosphate-sensing mechanism that when disrupted, inhibits degradation of HMG CoA reductase and triggers overproduction of corneal cholesterol that characterizes the eye disease Schnyder Corneal Dystrophy.
Genetic and biochemical studies show that a conserved ribosome biogenesis complex also localizes to heterochromatin, where it triggers RNA degradation and promotes the spreading and epigenetic inheritance of histone methylation.
The inhibition of sterol-accelerated degradation of HMG CoA reductase by the vitamin K2 synthetic enzyme UBIAD1 may contribute to the accumulation of cholesterol that is associated with Schnyder corneal dystrophy.
Under normal nutritional conditions, G-protein coupled receptors can control autophagy by regulating the degradation of key autophagic regulator Atg14L through ZBTB16-mediated ubiquitination and proteasome degradation.
The enzyme that collaborates with ubiquitin ligases to promote the release of defective polypeptides from stalled ribosomes in a process named ribosome-associated degradations has been identified as the ATPase Cdc48.
The human cytomegalovirus (HCMV) interactome systematically characterises high-confidence viral-viral and viral-host protein interactions in HCMV-infected cells, facilitating multiple novel insights into HCMV and herpesviral function.