BD Pharmingen™ Purified Mouse Anti-Human IKKβ w/ Control

Nuclear factor kappa B (NF-κB) is a ubiquitous transcription factor and an essential mediator of gene expression during activation of immune and inflammatory responses. The nuclear transcription factor kappa-B, NF-κB, is controlled by interaction with an inhibitory subunit, I-κB, which restricts NF-κB to the cytoplasm. Following stimulation by various cytokines or other stimuli, I-κB becomes degraded and NF-κB is released to the nucleus. The release of I-κB from NF-κB is thought to be a critical point in the activation of NF-κB signal pathways. A group of proteins form an NF-κB regulatory complex, or signalsome. Two members of this complex are a pair of closely related serine/threonine kinases, IKKα and IKKβ (also called IKK-1 and IKK-2), which phosphorylate critical residues of I-κB, thus targeting it for subsequent degradation. The IKK complex contains similar amounts of IKKα, IKKβ, as well as two other polypeptides, which are differentially processed forms of a third subunit, IKKγ. IKKα and IKKβ become activated following phosphorylation by upstream kinases, including NF-κB-inducing kinase (NIK) and MEKK1. IKKγ interacts preferentially with IKKβ and is required for the activation of the IKK complex. Experiments done on mice lacking IKKβ demonstrate that these mice died at mid-gestation from uncontrolled liver apoptosis. Furthermore, when cells  from IKKβ-deficient m ice were treated with tumor necrosis factor α or interleukin 1, neither IKK nor NF-κB were activated. Thus IKKβ, but not IKKα, plays a pivotal role in the induction of NF-κB and activation of IKK. IKKβ migrates at ~87 kDa in SDS/PAGE. The antibody recognizes human IKKβ. A recombinant protein corresponding to amino acids 1-666 of human IKKβ was used as the immunogen.