Coordinated expression of genes that regulate the survival, differentiation, and apoptosis of cells in the innate and adaptive immune systems is vital to ensure appropriate immune responses. One of the key transcription factors in both these immune systems is nuclear factor (NF)-κB. This transcription factor, which was initially identified as a nuclear factor binding to an enhancer region of the κ light chain of the immunoglobulin (Ig) gene in B cells [1], is now known to be expressed ubiquitously and become activated in response to various stimuli, including cytokines and bacterial or viral
JNJ 1661010 as well as different types of cellular stresses. NF-κB exists in an inactive cytosolic form as a complex with one of its inhibitor proteins, IκB-α, -β or -ε. Upon stimulation with any of a large number of inducers, NF-κB is rapidly activated via degradation of its associated inhibitor proteins and translocates into the nucleus, where it engages the transcription of its target
genes harboring a cognate κB enhancer element(s) [2] and [3]. Although numerous studies have provided solid evidence for critical roles of NF-κB, it remains to be elucidated how appropriate genes are selectively expressed by this multifunctional transcription factor, which is activated in various biological reactions.
