Nitric oxide (NO) is a signaling molecule that exerts a variety of regulatory functions in physiological states and stress responses. NO has been proposed to modulate protein function through S-nitrosylation of cysteine thiol residues in proteins. Appropriate amounts of NO result in neuroprotective effects via increasing moderate S-nitrosylated proteins and the cGMP pathway. On the other hand, excess amounts of NO promote neurodegenerative signaling pathways by increasing aberrant S-nitrosylated proteins.We found that Ras GTPase-activating protein-binding protein 1 (G3BP1), which forms stress granules (SGs) implicated in neurodegenerative diseases, was a target of S-nitrosylation. Treatment with NO stimulated this modification in a concentration-dependent manner. It has been known that SGs are rapidly formed by oxidative and heat shock stresses. In addition, SGs formation induced by proteasome inhibitor (MG132) was gradually degraded, whereas NO delayed this degradation. These findings suggest that S-nitrosylated G3BP1 not only promotes SGs formation but also delays SGs clearance.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.