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To view a copy of this licence, visit About this article Cite this article Xu, H., Chen, H., Li, Y

Krishnan and Nestler, 2008)

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(2021) reported that m6A modification appeared to enhance Beclin-1-mediated autophagy and consequently trigger ferroptosis in human HSCs, which is further confirmed by silencing YT521-B homology domain family, a critical m6A reader protein for sustaining Beclin-1 mRNA stability

Mitochondrial derived peptide literature, including work on MOTS c, has reinforced the value of linking signaling perturbations to downstream metabolic state signatures and stress response programs in model systems