In particular, a growing body of in vivo evidence supports the concept that some cancers become functionally dependent on FSP1, creating a therapeutic vulnerability that can be exploited either as monotherapy in specific contexts or as combination therapy with ferroptosis-inducing treatments
This difference in subcellular localization, combined with its distinct expression patterns, suggests that the two proteins play different roles in regulating cellular GSH levels (Ward et al., 2024)
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[DOI] [PubMed] [Google Scholar] 78.Harfield J.C., Batchelor-McAuley C., Compton R.G
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