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Overall, these results show that the level of SNO-CoA, rather than other NO donors, has primary control of the inhibition, supporting a CoA-delivered modification mechanism

Tissue-level deficiency of cobalamin is associated with an increase in the urinary and serum concentrations of an organic acid called methylmalonic acid, which is an alternative product of a cobalamin dependent pathway within the mitochondria

The PTEN-induced kinase 1 (PINK1)/Parkin pathway serves a pivotal role in the context of mitochondrial dysfunction and its association with PD