Application(s): positive control for WB · Source: recombinant enzyme expressed in E. coli and purified out of inclusion bodies · M_r: 74.5 kDa · Specific activity: 40 units/mg · Protein concentration: 0.5 mg/ml · The NF-κB/Rel family of transcription factors is comprised of several structurally-related proteins that form homodimers and heterodimers and include p50/p105, p52/p100, RelA (p65), and c-Rel/NF-κB ¹. Members of this family are responsible for regulating over 150 target genes, including the expression of inflammatory cytokines, chemokines, immunoreceptors, and cell adhesion molecules. Because of this, NF-κB has often been called a 'central mediator of the human immune response.² Acting as dimers, these transcription factors bind to 10 base pair DNA sequences, collectively called κB sites thereby regulating expression of target genes. The most common Rel/NF-κB dimer in mammals contains (p50)-RelA (p50/p65) heterodimers and is called NF-κB. The importance of Rel/NF-κB transcription factors in human inflammation and certain diseases makes them attractive targets for potential therapeutics.^3,4,5

1 Gilmore, T.D. The Rel/NF-κB signal transduction pathway: Introduction. Oncogene 18 6842-6844 (1999).

2 Pahl, H.L. Activators and target genes of Rel/NF-κB transcription factors. Oncogene 18 6853-6866 (1999).

3 Gilroy, D.W., Lawrence, T., Perretti, M., et al. Inflammatory resolution: New opportunities for drug discovery. Nat Rev Drug Discov 3 401-416 (2004).

4 Maeda, S., Hsu, L., Liu, H., et al. Nod2 mutation in Crohn’s disease potentiates NF-κB activity and IL-1β processing. Science 307 734-738 (2005).

5 Clark, A.G., and Debnam, P. Inhibition of glutathione S-transferases from rat liver by S-nitroso-L-glutathione. Biochem Pharmacol 37 3199-3201 (1988).

Gilmore, T.D. The Rel/NF-κB signal transduction pathway: Introduction. Oncogene 18 6842-6844 (1999).

Pahl, H.L. Activators and target genes of Rel/NF-κB transcription factors. Oncogene 18 6853-6866 (1999).

Maeda, S., Hsu, L., Liu, H., et al. Nod2 mutation in Crohn’s disease potentiates NF-κB activity and IL-1β processing. Science 307 734-738 (2005).

Arkan, M.C., Hevener, A.L., Greten, F.R., et al. IKK-β links inflammation to obesity-induced insulin resistance. Nat Med 11(2) 191-198 (2005).

Gilroy, D.W., Lawrence, T., Perretti, M., et al. Inflammatory resolution: New opportunities for drug discovery. Nat Rev Drug Discov 3 401-416 (2004).

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