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J. Biol. Chem., Vol. 278, Issue 47, 46541-46548, November 21, 2003

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Cytoplasmic IB Increases NF-B-independent Transcription through Binding to Histone Deacetylase (HDAC) 1 and HDAC3^*

Patrick Viatour, Sylvie Legrand-Poels, Carine van Lint¶, Michael Warnier, Marie-Paule Merville||, Jacques Gielen, Jacques Piette, Vincent Bours, and Alain Chariot||**

From the Laboratory of Medical Chemistry and Human Genetics and the Laboratory of Virology and Immunology, Center for Cellular and Molecular Therapy, University of Liège, Sart-Tilman, 4000 Liège, Belgium, and the ^¶Laboratory of Molecular Virology, Department of Biological Chemistry, Institute of Biological and Molecular Medicine, Free University of Brussels, 6041 Gosselies, Belgium

IB is an inhibitory molecule that sequesters NF-B dimers in the cytoplasm of unstimulated cells. Upon stimulation, NF-B moves to the nucleus and induces the expression of a variety of genes including IB. This newly synthesized IB also translocates to the nucleus, removes activated NF-B from its target genes, and brings it back to the cytoplasm to terminate the phase of NF-B activation. We show here that IB enhances the transactivation potential of several homeodomain-containing proteins such as HOXB7 and Pit-1 through a NF-B-independent association with histone deacetylase (HDAC) 1 and HDAC3 but not with HDAC2, -4, -5, and -6. IB bound both HDAC proteins through its ankyrin repeats, and this interaction was disrupted by p65. Immunofluorescence experiments demonstrated further that IB acts by partially redirecting HDAC3 to the cytoplasm. At the same time, an IB mutant, which lacked a functional nuclear localization sequence, interacted very efficiently with HDAC1 and -3 and intensively enhanced the transactivation potential of Pit-1. Our results support the hypothesis that the NF-B inhibitor IB regulates the transcriptional activity of homeodomain-containing proteins positively through cytoplasmic sequestration of HDAC1 and HDAC3, a mechanism that would assign a new and unexpected role to IB.

Received for publication, June 17, 2003 , and in revised form, August 29, 2003.

^* This work was supported by grants from the National Fund for Scientific Research, Belgium (F.N.R.S.) and TELEVIE and by the Belgian "Centre Anti-Cancéreux" (Ulg). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Part of a PAI (Pôle d'attraction inter-universitaire).

^|| Research Associate at the F.N.R.S.

^** To whom correspondence should be addressed: Laboratory of Medical Chemistry/CTCM, Pathology, +3 B23, C.H.U. Sart-Tilman, University of Liège, 4000 Liège, Belgium. Tel.: 32-4-366-24-86; Fax: 32-4-366-45-34; E-mail: Alain.chariot{at}ulg.ac.be.

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