All articles tagged with #s nitrosylation
Researchers identify S-nitrosylation of the immune protein STING at cysteine 148 as a driver of brain inflammation in Alzheimer's; blocking this switch in mice reduced inflammation and protected synapses, with the same pathway active in human Alzheimer’s samples and stem-cell models, suggesting a new therapeutic target that dampens harmful inflammation without shutting down normal immunity.
Researchers pinpoint S-nitrosylation of the STING protein at cysteine 148 as a driver of chronic brain inflammation and synapse loss in Alzheimer’s. In mouse models, preventing this modification reduced inflammation and protected synapses, a result mirrored in human Alzheimer’s tissue and stem-cell models. The findings suggest a targeted therapy that dampens harmful inflammation without suppressing overall immunity, with small molecules designed to block the cysteine-148 site in development.
Excess nitric oxide can modify TSC2 via S-nitrosylation, marking it for destruction and removing the mTOR 'brake.' With TSC2 diminished, mTOR activity surges, disrupting neuronal signaling in autism models. Blocking NO signaling or engineering a NO-resistant TSC2 normalized mTOR and improved related cellular readouts in SHANK3 and CNTNAP2 mouse models, and clinical samples from children with SHANK3 mutations and idiopathic ASD showed reduced TSC2 and elevated mTOR, supporting a NO–TSC2–mTOR mechanism and suggesting nitric oxide inhibitors as a potential ASD therapy and biomarker target.