Based on prior reports linking mitochondrial protein stability to a short fragment within the cyclic structural domain of SLC25A39 (amino acids 7286) that mediates glutathione (GSH) response and recruits SLC25A39 to AFG3L2 for proteolysis, we generated a deletion mutant lacking this fragment (aa72-86), confirmed by Sanger sequencing (Fig
Although some treatments can relieve symptoms in the short term, their overall effectiveness is still limited by a number of factors
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Furthermore, when the ratios of NAD + to NADH in wild-type and mutant strains were compared we detected a significantly lower ratio of NAD + to NADH in the gdh3/gdh3 mutant than in the wild-type strain when incubated in proline medium, while a higher ratio of NAD + to NADH in the gdh3/gdh3 mutant than in the wild-type strain in MM medium (Supplementary Fig
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