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To confirm that the diet-induced changes in CDO half-life observed in whole animals are due to regulation of CDO ubiquitination and degradation by the 26S proteasome, we explored CDO ubiquitination in response to diet in intact rats (Dominy et al

This phenotype was accompanied by accumulation of intracellular ferrous iron and lipid peroxides and the extracellular release of malondialdehyde, all indicative of redox stress, and increased levels of lactate dehydrogenase in the culture supernatant, indicating enhanced cell injury

10.1126/sciadv.1600031 34 EdwardsM

Increased cyclic AMP-dependent protein kinase activity in postmortem brain from patients with bipolar affective disorder

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