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5d) therefore suggests a less efficient interaction between E170X mutants and HEDS-derived GSSEtOH in accordance with the scaffold model and the hypothesis that GSSEtOH formation is catalysed by ScGrx7

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-Glutamylcyclotransferase (GGCT), a key metabolic enzyme frequently overexpressed in various cancers, has an undefined role in directing glutamine metabolic flux during tumorigenesis

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