IKKβ (human, recombinant)

IĸB kinase β (IKKβ) is a catalytic subunit of the IĸB kinase (IKK) complex, a key mediator of NF-κB activation.¹ It is composed of an N-terminal kinase domain, which contains an activation loop with two serine residues, Ser 177 and Ser 181, that are subject to phosphorylation, a ubiquitin-like domain, a scaffold dimerization domain, and a C-terminal domain that binds the regulatory subunit IKKγ, also known as NF-κB essential modifier (NEMO). IKKβ is ubiquitously expressed and localizes in the cytoplasm to the IKK complex, which mediates NF-κB activation in response to numerous stimuli, including inflammatory cytokines and B- and T cell receptor engagement, as well as LPS and growth factors. Upon cellular stimulation, the TAK1-TAB complex phosphorylates and activates IKKβ, which induces phosphorylation and degradation of the NF-κB inhibitory protein IĸB, permitting NF-κB nuclear translocation and the transcription of numerous genes involved in inflammation, immunity, and cell survival and proliferation.^2,1 IKKβ has roles in several pathological conditions, including cancer and inflammatory diseases, such as rheumatoid arthritis.¹ IKBKB mutations have been found in patients with severe combined immunodeficiency (SCID).³ Cayman’s IKKβ (human, recombinant) protein can be used for enzyme activity assays.

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1. Prescott, J.A., and Cook, S.J. Targeting IKKβ in cancer: Challenges and opportunities for the therapeutic utilisation of IKKβ inhibitors. Cells 7(9), 115 (2018).

2. Yu, H., Lin, L., Zhang, Z., et al. Targeting NF-κB pathway for the therapy of diseases: Mechanism and clinical study. Signal Transduct. Target. Ther. 5(1), 209 (2020).

3. Pannicke, U., Baumann, B., Fuchs, S., et al. Deficiency of innate and acquired immunity caused by an IKBKB mutation. N. Engl. J. Med. 369(26), 2504-2514 (2013).