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To sustain the genome stability, cells have evolved a complicated fine-tuning mechanism, termed as DNA-damage response (DDR), to detect and repair DNA lesions

Indeed translocation of mTORC1 from the cytoplasm to the lysosome, a rich compartment in amino acids, is critical for mTORC1 activation ( per se is also able to regulate mTORC1 activity ( In brief, activation of the GCN2-ATF4 amino acid stress pathway and inhibition of protein synthesis through inhibition of mTORC1 demonstrates the strong proteogenic role played by cysteine in tumor cells

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Same molecules, same mechanism, entirely different philosophy

This modification uniquely induces structural rearrangements associated with amyloidogenic conversion, in contrast to other post-translational modifications on Cys10, such as, S-cysteinylation or S-glutathionylation, that do not significantly alter the native fold [22]

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