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In order to investigate if the substrate binding protein of Gsi (GsiB) transfers GSH to Opp or vice versa (OppA to Gsi), we generated GSH-deficient cells lacking either OppA and GsiC or GsiB and OppC and expressed Grx1-roGFP2 in the resulting Δ gshA Δ gsiB Δ oppC and Δ gshA Δ oppA Δ gsiC triple mutants (see Figure 7 A for a schematic overview)

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In summary, ferroptosis-based models reveal the complex regulatory landscape of PC and hold promise for clinical translation

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