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

Abstract We have cloned the cDNA encoding IκB-β, one of the two major IκB isoforms in mammalian cells. The recombinant IκB-β 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 IκB-α and IκB-β is in their response to different inducers of NF-κB activity. One class of inducers causes rapid but transient activation of NF-κB by primarily affecting IκB-α complexes, whereas another class of inducers causes persistent activation of NF-κB by affecting both IκB-α and IκB-β complexes. Therefore, the overall activation of NF-κB consists of two overlapping phases, a transient phase mediated through IκB-α and a persistent phase mediated through IκB-β.