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J. Biol. Chem., Vol. 281, Issue 6, 3389-3397, February 10, 2006

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Differential Use of Functional Domains by Coiled-coil Coactivator in Its Synergistic Coactivator Function with -Catenin or GRIP1^*

Catherine K. Yang, Jeong Hoon Kim¹, Hongwei Li, and Michael R. Stallcup²

From the Departments of Biochemistry and Molecular Biology and of Pathology, University of Southern California, Los Angeles, California 90089

-Catenin, a pivotal component of the Wnt-signaling pathway, binds to and serves as a transcriptional coactivator for the T-cell factor/lymphoid enhancer factor (TCF/LEF) family of transcriptional activator proteins and for the androgen receptor (AR), a nuclear receptor. Three components of the p160 nuclear receptor coactivator complex, including CARM1, p300/CBP, and GRIP1 (one of the p160 coactivators), bind to and cooperate with -catenin to enhance transcriptional activation by TCF/LEF and AR. Here we report that another component of the p160 nuclear receptor coactivator complex, the coiled-coil coactivator (CoCoA), directly binds to and cooperates synergistically with -catenin as a coactivator for AR and TCF/LEF. CoCoA uses different domains to bind GRIP1 and -catenin, and it uses different domains to transmit the activating signal to the transcription machinery, depending on whether it is bound to GRIP1 or -catenin. CoCoA associated specifically with the promoters of transiently transfected and endogenous target genes of TCF/LEF, and reduction of the endogenous CoCoA level decreased the ability of TCF/LEF and -catenin to activate transcription of transient and endogenous target genes. Thus, CoCoA uses different combinations of functional domains to serve as a physiologically relevant component of the Wnt/-catenin signaling pathway and the androgen signaling pathway.

Received for publication, September 22, 2005 , and in revised form, November 29, 2005.

^* This work was supported in part by National Institutes of Health Grant DK43093 (to M. R. S.). 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.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1 and S2.

¹ Supported by a predoctoral fellowship from the University of Southern California/Norris Cancer Center Breast Cancer Research Training Program.

² To whom correspondence should be addressed: Dept. of Pathology, HMR 301, University of Southern California, 2011 Zonal Ave., Los Angeles, CA 90089-9092. Tel.: 323-442-1289; Fax: 323-442-1224; E-mail: stallcup{at}usc.edu.

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