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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Transcriptional activation by NF-kappaB requires multiple coactivators.

Nuclear factor-kappaB (NF-kappaB) plays a role in the transcriptional regulation of genes involved in inflammation and cell survival. In this report we demonstrate that NF-kappaB recruits a coactivator complex that has striking similarities to that recruited by nuclear receptors. Inactivation of either cyclic AMP response element binding protein (CREB)-binding protein (CBP), members of the p160 family of coactivators, or the CBP-associated factor (p/ CAF) by nuclear antibody microinjection prevents NF-kappaB-dependent transactivation. Like nuclear receptor-dependent gene expression, NF-kappaB-dependent gene expression requires specific LXXLL motifs in one of the p160 family members, and enhancement of NF-kappaB activity requires the histone acetyltransferase (HAT) activity of p/ CAF but not that of CBP. This coactivator complex is differentially recruited by members of the Rel family. The p50 homodimer fails to recruit coactivators, although the p50-p65 heterodimeric form of the transcription factor assembles the integrator complex. These findings provide new mechanistic insights into how this family of dimeric transcription factors has a differential effect on gene expression.[1]

References

  1. Transcriptional activation by NF-kappaB requires multiple coactivators. Sheppard, K.A., Rose, D.W., Haque, Z.K., Kurokawa, R., McInerney, E., Westin, S., Thanos, D., Rosenfeld, M.G., Glass, C.K., Collins, T. Mol. Cell. Biol. (1999) [Pubmed]
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