The transcription factor NF-κB is a critical regulator of immune responses. To 
determine how NF-κB builds transcriptional control networks, we need to obtain a 
topographic map of the factor bound to the genome and correlate it with global 
gene expression. We used a ChIP cloning technique and identified novel NF-κB 
target genes in response to virus infection. We discovered that most of the 
NF-κB-bound genomic sites deviate from the consensus and are located away from 
conventional promoter regions. Remarkably, we identified a novel abundant 
NF-κB-binding site residing in specialized Alu-repetitive elements having the 
potential for long range transcription regulation, thus suggesting that in 
addition to its known role, NF-κB has a primate-specific function and a role in 
human evolution. By combining these data with global gene expression profiling 
of virus-infected cells, we found that most of the sites bound by NF-κB in the 
human genome do not correlate with changes in gene expression of the nearby 
genes and they do not appear to function in the context of synthetic promoters. 
These results demonstrate that repetitive elements interspersed in the human 
genome function as common target sites for transcription factors and may play an 
important role in expanding the repertoire of binding sites to engage new genes 
into regulatory networks.