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376 Ceruloplasmin deficiency results in brain iron overload and neurotoxicity

Recent studies have revealed an autoregulatory mechanism whereby mitochondrial GSH (mtGSH) homeostasis is controlled through a feedback loop involving solute carrier family 25 member 39 (SLC25A39) transporter and mitochondrial protease AFG3 like matrix AAA peptidase subunit 2 (AFG3L2), coupling GSH levels to iron-sulfur cluster biogenesis 16,17

Through mutation analysis, the active serine residue for hydrolase activity was defined, and mutation of this residue appeared to affect expression of COL1A1

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Irish J Med Sci

Verma, V