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Electrophiles inhibit NF-κB activity by binding to the p50 and RelA/p65 protein subunits. Michael addition at cysteine moieties prevent nuclear translocation required for target gene expression. Under inflammatory conditions, kinase activity induced by upstream NF-κB signaling results in phosphorylation, ubiquitinylation, and proteasomal degradation of IκB. Subsequently, NF-κB translocates to the nucleus to initiate target gene expression.
