Human IKK2 Xpress Clones
NF-kappa-B and REL proteins form the NF-kappa-B complex, which is inhibited by I-kappa-B proteins (including NFKBIA or NFKBIB). Binding of IκB will trap the NFκB complex in the cytoplasm. Phosphorylation on serine residues on the IkB protein by IKK1 or IKK2 will mark the protein for destruction via the ubiquitination pathway and allow the relocation of the NFkB complex to the nuclei for transcription functionalities. IKK1 or IKK2 may form homo- or hetero-dimer. The K44A or K44M mutation renders the protein kinase enzymatically inactive. The S177E / S181E mutant is potentially constitutively active while S177A / S181A mutant can no longer be activated by upstream kinases.
