K739 is preferentially targeted over K725 in the deSUMOylation process of neuronal nitric oxide synthase
N0 mitigated ischemia-induced damage in the MCAO model, unlike N2 and N3, suggesting moderate CaMBD affinity prevents excessive nNOS activation and aberrant SUMOylation at K739, critical for neuroprotection. Stronger SENP1 binding at K739 supports targeted deSUMOylation strategies. Further research is needed to optimize peptide therapies and clarify CaM-SUMOylation interactions for nNOS-related disorders.
Authors
- Nan Wang (ORCID: https://orcid.org/0000-0001-7129-6089)
- Yuxin Xu
- Wei Wan (ORCID: https://orcid.org/0000-0001-9462-5615)
Institutions
- Xuzhou Medical College (CN)
Publication Details
- Journal
- Frontiers in Chemistry
- Published
- 2025-09-04
- DOI
- https://doi.org/10.3389/fchem.2025.1672437
- Primary Topic
- Redox biology and oxidative stress
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China
- Xuzhou Medical University