Drosophila genetics and behavior reveal that oxidative stress induced axonal degeneration in a single class of neurons drives the functional decline of an entire neural network and the behavior it controls.

The ATM kinase has an unanticipated role in tumor progression through the regulation of cell migration by oxidative stress.

Direct modification by endogenous peroxide of a conserved cysteine in the molecular chaperone BiP decouples its ATPase and peptide-binding activities, allowing for enhanced polypeptide holdase activity during oxidative stress.

In response to tissue damage, reactive oxygen species can be sensed by cation channels TRPA1/RyR to cause increases of cytosolic Ca²⁺ in intestinal stem cells, activating Ras/MAPK activity and stimulating stem cell proliferation in Drosophila.

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

By contributing to the maintenance of ROS homeostasis, CD33-related Siglecs control oxidative damage and influence rate of aging and lifespan.

SAK1, a novel cytoplasmic phosphoprotein, is a key intermediate component of the retrograde signaling pathway controlling nuclear gene expression during acclimation of Chlamydomonas cells to singlet oxygen stress.

A sudden fall in the levels of the coenzyme NADPH within cells could have a central role in the process of aging.

Building on previous work (Wang et al., 2014), it is shown that the nucleotide exchange factor of the chaperone BiP (Sil1) unexpectedly facilitates the reduction of oxidized BiP.

Oxidative stress leads to the translocation of Rab5 from endosome to mitochondria, regulated by ALS/Alsin, a component associated with amyotrophic lateral sclerosis, leading to mitochondrial-endosomal physical contacts and a cytoprotective response.