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The entire 4b helix shifts βΌ1 Γ in comparison to the 1EEM structure due to the sulfonamide group interacting with three residues (G128, V127 and P124) within the helix
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This is important for the development of vascular lesion because it shows that G6PD deficiency, while reducing the reactive nitrogen species, actually increases the production of ROSs that exert much more deleterious effects than NO itself [46]
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