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This makes melanocytes relatively vulnerable to oxidative stress [23]

In summary, SLC7A5 overexpression was able to reverse the protective effects of YTHDF1 knockdown, revealing the critical role of SLC7A5 in the YTHDF1-mediated cytoprotective mechanism

Nat Commun (2021) 12(1):3073

The resultant surplus of glutamate excessively stimulates NMDA receptors on spinal neurons, resulting in calcium influx, oxidative damage, and neuronal hyperexcitability [65, 117]