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This small molecule exists mainly in two forms: reduced (GSH) and oxidized (GSSG)

The molecular mechanism by which the PfK13 mutations confer artemisinin resistance in clinical isolates may involve multiple cellular and metabolic processes, including hemoglobin uptake and digestion, the unfolded protein stress response, mitochondrial functions, oxidative stress responses (including tRNA thiouridine modification reprogramming), and an enhanced DNA damage repair mechanism 3, 811, 1320

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