The chloroplast 2-cysteine peroxiredoxin is central player and missing link in the chloroplast thiol-disulfide redox regulatory network, and participates in oxidative inactivation of reductively activated enzymes in photosynthesis.
The use of genetically encoded redox sensors in phagocytized bacteria reveals that, among the toxic cocktail of oxidants released into the neutrophil's phagolysosome, HOCl is the main component responsible for the oxidative modification of bacterial protein thiols.
Proinsulin misfolding, an established cause of diabetes in patients with INS gene mutations, is now observed in normal human pancreatic islets, and rodents with genetic predisposition to type 2 diabetes.
Non-invasive mRNA stability measurements reveal that transcript lifetime is governed by a competition with translation initiation on a transcriptome-wide level.
ATF4, the master regulator of transcription during the Integrated Stress Response (ISR), causes global changes in cysteine sulfhydration of proteins and this event causes cellular metabolic reprogramming.
The ES6S region of the small subunit ribosome makes a place for the threading and secondary structure unwinding of mRNA, which regulates genome-wide translation.
Reducing Akt-mediated huntingtin phosphorylation decreases APP accumulation at the synapse by reducing its anterograde axonal transport and ameliorates learning and memory in a mouse model of familial Alzheimer disease.
The major protein disulfide isomerase family member, PDIA1, is essential in beta cells of mice fed a high-fat diet to maintain glucose homeostasis, proinsulin maturation and organelle integrity.
The major cytosolic yeast peroxiredoxin Tsa1 controls aging and H2O2-resistance by inhibiting protein kinase A through a conserved cysteine in the catalytic subunit activation loop and not by scavenging H2O2.
