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The two tricarballylic acid moieties are essential for toxicity and they can be removed by hydrolysis of the ester bonds catalyzed by carboxylesterases present in bacteria and fungi

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In GPx1-deficient human endothelial cells, we found that NFκB mediated the inflammatory activation at baseline, although there is a role for NFκB and MAPK pathways (c-Jun N-terminal kinase or JNK and ERK1/2) in the augmented responses of these cells to TNFα as well [6]