Overview:

Nuclear Factor kappa B (NF-kB) is a ubiquitous transcription factor and an essential mediator of gene expression during the activation of immune and inflammatory responses. NF-kB mediates the expression of a great variety of genes in response to extracellular stimuli. NF-kB is associated with IkB proteins in the cytoplasm of the cell, which inhibit NF-kB activity.  IkB proteins are phosphorylated by an IkB kinase complex consisting of at least three proteins, IKKa, IKKb, and IKKg.   Isolated from a cDNA library of LPS-stimulated mouse macrophage cells, a novel molecule in the IKK complex has been recently identified and designated IKKi and/or IKKe. IKKepsilon is required for the activation of NF-kB by mitogens and T cell receptors but not by TNFa or IL-1.  LPS increases the IKKe mRNA level in mouse macrophage cell lines. This protein has significant sequence homology with kinase domains of IKKa and IKKb. Overexpression of wild type IKKe in cells phosphorylates Ser32 and Ser36 of IkBa. Anti-IKKe pT501 antibody is ideal for investigators involved in NFkappaB and apoptosis reasearch.

References:

1. Sweeney SE, et al.: Antiviral gene expression in rheumatoid arthritis: role of IKKepsilon and interferon regulatory factor 3. Arthritis Rheum. 2007: 56(3); 743-752.