passages: PMID-21189157__text
passages: abstract
passages: ZAS3 represses NFkappaB-dependent transcription by direct competition for DNA binding. 
  NFkappaB and ZAS3 are transcription factors that control important cellular processes including immunity, cell survival and apoptosis. Although both proteins bind the kappaB-motif, they produce opposite physiological consequences; NFkappaB activates transcription, promotes cell growth and is often found to be constitutively expressed in cancer cells, while ZAS3 generally represses transcription, inhibits cell proliferation and is downregulated in some cancers. Here, we show that ZAS3 inhibits NFkappaB-dependent transcription by competing with NFkappaB for the kappaB-motif. Transient transfection studies show that N-terminal 645 amino acids is sufficient to repress transcription activated by NFkappaB, and that the identical region also possesses intrinsic repression activity to inhibit basal transcription from a promoter. Finally, in vitro DNA-protein interaction analysis shows that ZAS3 is able to displace NFkappaB by competing with NFkappaB for the kappaB-motif. It is conceivable that ZAS3 has therapeutic potential for controlling aberrant activation of NFkappaB in various diseases.
  