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.
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.
NEIL DNA glycosylases are required to counteract oxidative base damages within the mitochondrial genome to safeguard neural crest cell differentiation.
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.
The important role of serine biosynthesis in Müller cells may explain why the macula is so much more prone to developing disease than the rest of the retina.
Genetic analysis reveals NADPH oxidase generated reactive oxygen species as signals to re-establish cellular homeostasis during aging via activating a transcriptional response.
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.
Development and application of highly sensitive in situ transcriptomics method, Flura-seq, in identifying dynamic organ-specific transcriptomes in early stage breast cancer metastasis have been described.
