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Site-directed mutagenesis and inhibition assays revealed that Phe-9 is potentially an important residue for the binding of the inhibitor S-hexyl glutathione (GTX) 77
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This action is reminiscent of dimethyl fumarate (DMF), an approved MS therapy, which also downregulates pro-inflammatory cytokines like IL-1β and TNF-α through microglial modulation [87,88]
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