IκB-β regulates the persistent response in a biphasic activation of NF-κB

We have cloned the cDNA encoding IKB-I~, one of the two major IKB isoforms in mammalian cells. The recombinant IKB-p protein interacts with equal affinity to p65 and c-Rel and does not exhibit a preference between these Rel proteins, instead the primary difference between IKB-a and IKB-I~ iS in their response to different inducers of NF-KB activity. One class of inducers causes rapid but transient activation of NF-KB by primarily affecting IKB-e complexes, whereas another class of inducers causes persistent activation of NF-KB by affecting both IKB-a and IKB-J~ complexes. Therefore, the overall activation of NF-KB consists of two overlapping phases, a transient phase mediated through IKB-(L and a persistent phase mediated through IKB-I~.