The NF-κB/Rel signaling pathway includes NF-κB2 p52/p100, NF-κB1 p50/p105, c-Rel, RelA/p65, and RelB. These proteins act as dimeric transcription factors that control gene regulation in various biological processes, including innate and adaptive immunity, inflammation, stress response, B cell development, and lymphoid organogenesis. In the classical or non-classical pathways, NF-κB/Rel proteins are bound and inhibited by IκB proteins. Pro-inflammatory cytokines, LPS, growth factors, and antigen receptor activation stimulate the IKK complex (IKKβ, IKKα, and NEMO), leading to phosphorylation of IκB proteins. Phosphorylation of IκB results in its ubiquitination and proteasomal degradation, releasing the NF-κB/Rel complex. The active NF-κB/Rel complex is further activated by phosphorylation and translocated into the nucleus, inducing the expression of target genes.The NFKB Reporter TF-1 Cell Line is a Luciferase reporter gene cell line. Upon binding of TNF-α to its receptor, downstream signaling pathways are activated, leading to the expression of Firefly Luciferase. Luciferase readings represent the activation effect of the signaling pathway and can be used for evaluating the activation effect of TNF-α.
