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This paper presents the first demonstration that transplanted oligodendrocytes can form new myelin, using a naturally occurring mouse mutant that lacks normal myelin as a result of the loss of myelin basic protein, a protein essential for the compaction of the myelin sheath

[1] TML is then hydroxylated into hydroxytrimethyllysine (HTML) by trimethyllysine dioxygenase (TMLD), requiring the presence of ascorbic acid and iron

However, numerous studies have shown that solely depleting extracellular cystine or inhibiting cystine uptake by xCT inhibitors such as Erastin or Imidazole Ketone Erastin (IKE) is enough to result in the depletion of intracellular cysteine and GSH pools, subsequently, the inactivation of GPX4 and the accumulation of peroxidized phospholipids, thereby the induction of ferroptosis 1,9,21

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