NF-κB, Nrf2, Keap1

Although NF-κB, Nrf2, and Keap1 are critically linked in cellular stress and inflammation signaling (including reciprocal crosstalk), they represent three distinct molecules, each with different canonical names and mechanisms. Referencing them collectively is non-standard and should be split into separate entries for information structuring. NF-κB is the principal mediator of inflammatory gene expression; Nrf2 is the principal mediator of cytoprotective antioxidant gene expression; Keap1 is the regulator/inhibitor of Nrf2. Drugs may target these pathways in a complementary manner for inflammatory or degenerative diseases, but structurally and functionally they are distinct. Listing “NF-κB, Nrf2, Keap1” as one target is non-canonical. For structured information, treat each molecule/receptor separately.

NF-κB is the principal mediator of inflammatory gene expression; Nrf2 is the principal mediator of cytoprotective antioxidant gene expression; Keap1 is the regulator/inhibitor of Nrf2. Drugs may target these pathways in a complementary manner, but structurally and functionally they are distinct.