Mouse Inhibitory Subunit of NF Kappa B Alpha (IkBa) ELISA Kit-Sandwich

NF-kappa-B inhibitor alpha (IκBα) functions by inhibiting dimeric NF-kappa-B/REL complexes, trapping REL dimers (RELA/p65 and NFKB1/p50) in the cytoplasm by concealing their nuclear localization signals. Upon cellular stimulation during immune and pro-inflammatory responses, IκBα becomes phosphorylated, leading to its ubiquitination and degradation. This process allows the dimeric RELA to move to the nucleus and activate transcription. IκBα is a crucial regulator of NF-κB in mice, essential for maintaining immune balance and preventing inflammatory diseases. In mouse macrophages, IκBα degradation is commonly linked with the swift activation of NF-κB. For instance, under lipopolysaccharide (LPS) stimulation, IκBα is rapidly degraded, freeing NF-κB to translocate to the nucleus and activate target genes.