coli was improved by the modification of metabolic pathways, including the reduction of l-cysteine degradation, manipulation of the glucose storage pathway, and elimination of the biological degradation of GSH
Conversely, copper deficiency elevates the risk of atherosclerosis by increasing cholesterol levels and reducing the activity of the copper-dependent antioxidant enzyme SOD1
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Network pharmacology and molecular docking suggested CA9 as a putative binding target of ATT-I which was confirmed by CETSA demonstrating increased thermal stability of CA9 upon ATT-I treatment