Endoplasmic reticulum stress in yeast activates not only the UPR but also Rpn4, promoting the clearance of misfolded proteins from the cytosol as part of a modular cross-compartment stress response.

fmo-4 slows aging downstream of dietary restriction and mTOR and regulates calcium-mediated signaling in the hypodermis.

In a chemical genetics study, JM03 derived from crotamiton, an inhibitor of trainsient receptor potential vanilloid-4 channels, was identified to extend lifespan and improve oxidative and hypertonic stress resistance in Caenorhabditis elegans via inhibiting OSM-9.

Oncoprotein BCL6 confers tumor adaptive resistance to genotoxic stress through the IFN-BCL6-PTEN axis in solid tumors and presents a promising combinational target for chemo-sensitization.

Separate genetic pathways mediate longevity, pathogen resistance, and cell-nonautonomous regulation of xenobiotic detoxification in chemosensory defective Caenorhabditis elegans mutants.

Most of the mRNAs whose translation is resistant to the stress-induced repression of protein synthesis contain upstream open reading frames that are efficiently translated under normal conditions.

Genetic analysis reveals NADPH oxidase generated reactive oxygen species as signals to re-establish cellular homeostasis during aging via activating a transcriptional response.

In nematode worms, NSUN-1 methylates ribosomal RNA and influences phenotypes related to aging, stress resistance, germ line development, and cuticle integrity by regulating translation of specific mRNAs.

Mutations in several components of a bacterial ribosome are shown to broadly decrease antibiotic and stress sensitivity, and readily accessible reversion mutations allow these ribosomal mutations to serve as stepping stones to high level antibiotic resistance.

Nonlinear H₂O₂ scavenging by peroxiredoxins drives acquired stress resistance and replicative lifespan hormesis.