BD Pharmingen™ Purified Mouse Anti-Human IκBα

NF-κB is a transcription factor which is a member of the mammalian NF-κB/Rel family of proteins. Members of this family are involved in the regulation of cell proliferation, immune function, as well as development. NF-κB is normally found in the cytoplasm and remains in an inactive state by its association with an inhibitory protein, IκB. Stimulation of NF-κB by a variety of inducers causes the degradation of IκBs and translocation of NF-κB to the nucleus and activation of the target gene. IκBα is a member of the IκB family of proteins, including IκBβ, IκBγ, Bcl-3, and the precursors of NF-κB1 (p105), and NF-κB2 (p100). IκBα is the best characterized member of the family and has been shown to contain three different structural domains: an N-terminal region, an amino acid internal region containing ankyrin repeats, and a C-terminal region containing a PEST domain. In resting cells, IκBα binds to and maintains NF-κB in the cytoplasm by blocking the nuclear localization sequences of NF-κB. In response to an extracellular signal, IκBα is phosphorylated and subsequently degraded via the ubiquination-proteasome pathway, allowing NF-κB to translocate to the nucleus. Once in the nucleus, NF-κB can induce the transcription of IκBα thereby renewing the cycle so that IκBα can form a complex with NF-κB and maintain it in its cytoplasmic location. IκBα -/- mice have been shown to die soon after birth and show an increased level NF-κB activity. Furthermore, in Hodgkin's lymphoma (HL) a high constitutive level of NF-κB has been reported in samples in which clonal deleterious mutations were detected in the IκBα plays in the pathogenic process which leads to HL remains to be elucidated. IκBα migrates at ~40 kDa in SDS/PAGE, while the deduced molecular weight based upon its cDNA sequence is ~36 kDa (SWISS PROT Accession number P25963).