eNOS-dependent S-nitrosylation of the NF-κB subunit p65 has neuroprotective effects

• DOI: 10.1038/s41419-020-03338-4
• Publication Date: 2021-01-07T20:03:40Z
• Authors: Ariel Caviedes; Barbara Maturana; Katherina Corvalán; Alexander Engler; Felipe Gordillo; Manuel Varas-Godoy; Karl-Heinz Smalla; Luis Federico Batiz; Carlos Lafourcade; Thilo Kaehne; Ursula Wyneken
• Keywords: Excitotoxicity; S-Nitrosylation

Abstract Cell death by glutamate excitotoxicity, mediated N -methyl- d -aspartate (NMDA) receptors, negatively impacts brain function, including but not limited to hippocampal neurons. The NF-κB transcription factor (composed mainly of p65/p50 subunits) contributes neuronal in while its inhibition should improve cell survival. Using the biotin switch method, subcellular fractionation, immunofluorescence, and luciferase reporter assays, we found that NMDA-stimulated activity selectively neurons, endothelial nitric oxide synthase (eNOS), an enzyme expressed is involved S-nitrosylation p65 consequent cerebrocortical, i.e., resistant S-nitro proteomes cortical neurons revealed different biological processes are regulated susceptible bringing light protein a ubiquitous post-translational modification, able influence variety homeostatic transcriptional exposed NMDA receptor overstimulation.