S-nitros(yl)ation of CaMKIIα and its precision redox regulation by SNOTAC plays a critical role in learning and memory.

ABSTRACT: Ca²⁺/calmodulin-dependent protein kinase II α (CaMKIIα) and nitric oxide (NO) both play vital roles in learning and memory; however, the underlying mechanisms connecting them have remained elusive. To address this question, our study surprisingly observed that during learning and memory tasks, S-nitrosation of CaMKIIα, a key redox-based post-translational modification, significantly increased in mouse hippocampus. We then constructed mice with mutations in the major S-nitrosation sites of CaMKIIα (C280/289V) and found that the mutant mice exhibited remarkable cognitive impairments and attenuated long-term potentiation (LTP). Mechanistically, we demonstrated that the SNO-CaMKIIα mutation increased presynaptic release probability by increasing the interaction and the phosphorylati

SUBMITTER: Chu B 

PROVIDER: S-EPMC12540040 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature