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Molecular and Cellular Biology, September 1999, p. 6367-6378, Vol. 19, No. 9
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Transcriptional Activation by NF-kappa B Requires Multiple Coactivators

Kelly-Ann Sheppard,1 David W. Rose,2 Zaffar K. Haque,1 Riki Kurokawa,3 Eileen McInerney,4 Stefan Westin,3 Dimitris Thanos,5 Michael G. Rosenfeld,4 Christopher K. Glass,3 and Tucker Collins1,*

Vascular Research Division, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 021151; Department of Medicine and Whittier Diabetes Program,2 Division of Cellular and Molecular Medicine, Department of Medicine,3 and Howard Hughes Medical Institute,4 University of California---San Diego, La Jolla, California 92093; and Department of Biochemistry and Molecular Biophysics, Columbia University, New York, New York 100325

Received 19 January 1999/Returned for modification 1 June 1999/Accepted 21 June 1999

Nuclear factor-kappa B (NF-kappa B) plays a role in the transcriptional regulation of genes involved in inflammation and cell survival. In this report we demonstrate that NF-kappa B 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-kappa B-dependent transactivation. Like nuclear receptor-dependent gene expression, NF-kappa B-dependent gene expression requires specific LXXLL motifs in one of the p160 family members, and enhancement of NF-kappa B 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.

* Corresponding author. Mailing address: Department of Pathology, Brigham and Women's Hospital, 221 Longwood Ave., Boston, MA 02115. Phone: (617) 732-5990. Fax: (617) 278-6990. E-mail: tcollins{at}bustoff.bwh.harvard.edu.

Molecular and Cellular Biology, September 1999, p. 6367-6378, Vol. 19, No. 9
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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