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doi: 10.1021/acschemneuro.3c00127 214 SaundersN
[DOI] [PubMed] [Google Scholar] 105.Chiechio S, Copani A, Nicoletti F, Gereau RWt
Further, these data suggest that at acute time points following Gclc genetic deletion, compensation by NRF1 could be responsible for the dispensable role of NRF2 in GSH-depleted conditions
These ubiquitin modifications stabilize Complex I at the plasma membrane and create a scaffold for the recruitment of downstream signaling molecules, thereby promoting the activation of pro-survival NF-B signaling cascades
