Endoplasmic reticulum proteostasis factors enhance the mutational tolerance of influenza hemagglutinin, a model secretory pathway protein and therapeutic target, particularly improving the fitness of temperature-sensitive variants.

METTL18 methylates histidine 245 of ribosomal protein RPL3, retards ribosome traversal at tyrosine codons, and thus ensures nascent protein folding for proteostasis maintenance.

Stem cell-derived motor neurons with differential ALS vulnerability identified proteasome activity as a possible mechanism that explains their differential sensitivity.

Analysis of the mechanism of action of cystic fibrosis corrector drugs reveals signalling pathways potently controlling the proteostasis of the main disease-relevant CFTR mutant.

A time-resolved analysis of protein and RNA concentrations and interactions during proteostasis stress highlights the dominant role of translation regulation and a shift of energy metabolism.

Endo-siRNAs slow down the rate of aging and enable the maintenance of a responsive heat shock response in aging germline-less Caenorhabditis elegans.

The interaction between rDNA instability and proteostasis stress, two major aging hallmarks, underlies single-cell aging trajectories in yeast.

By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.

A novel co-translational mechanism continuously adjusts the expression levels of ribosomal proteins Rpl3 and Rpl4 to their consumption during ribosome synthesis by regulating the abundance of their mRNAs.

High-throughput screening of over 6000 drugs using cells and retina tissue with a CEP290 ciliopathy mutation identified a small molecule, reserpine, which enhanced photoreceptor survival in retinal organoids and in a mouse disease model by partially restoring balance in proteostasis.