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Cullen et al

Interestingly, BSO treatment did not affect SLC25A39 mRNA levels (Extended Data Fig 1c), but could induce SLC25A39 protein accumulation when an SLC25A39 cDNA lacking UTR elements was expressed ectopically under a viral promoter (Extended Data Fig 1d), thereby suggesting regulation at the post-translational level

In summary, our results suggest that DMP-mediated GSH elevation by a novel post-translational mechanism can inhibit neuronal hyperexcitability both in-vitro and in-vivo and a plausible link is the redox sensitive mTORC1 pathway