NFKBID (F8U2O) Rabbit Monoclonal Antibody #71044

The transcriptional activity of the nuclear factor κB (NF-κB) pathway is tightly regulated in various ways, primarily by post-translational modifications of REL proteins in addition to regulation by atypical members of the IκB protein family (1-4). Atypical IκB proteins of the Bcl-3 subfamily, which include Bcl-3, IκBζ, and NFKB inhibitor delta (NFKBID) (2), are not ubiquitinated and degraded after NF-κB activation; rather, they are highly expressed, acting as transcriptional regulators by binding to NF-κB transcription factors in the nucleus (3,4).

Like other IκBs, NFKBID and other atypical IκBs contain ankyrin repeats in their structure and act to modulate the NF-κB pathway. However, unlike typical IκB proteins, they do not actively repress nuclear localization of NF-κB proteins (1-5). NFKBID can change NF-κB-mediated transcription in a few ways: regulation of dimer formation, recruitment of histone-modifying enzymes, or stabilization of NF-κB proteins binding to DNA (5).

NFKBID is the smallest member of the Bcl-3 subfamily (6). NFKBID has been shown to interact with several different NF-κB dimers in the nucleus and plays a role in regulatory T cell (Treg) development in the thymus (7). NFKBID is important for IL-2-mediated stimulation of CD4 and CD8 cells (8). Mice deficient for NFKBID or c-REL show similar defects in adaptive and innate immune cell function (9,10).