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J. Biol. Chem., Vol. 278, Issue 28, 26135-26145, July 11, 2003

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Interaction between Smad-interacting Protein-1 and the Corepressor C-terminal Binding Protein Is Dispensable for Transcriptional Repression of E-cadherin^*

Leo A. van Grunsven, Christine Michiels, Tom Van de Putte, Luc Nelles, Gunther Wuytens, Kristin Verschueren  and Danny Huylebroeck

From the Department of Developmental Biology (VIB7), Flanders Interuniversity Institute for Biotechnology (VIB) and Laboratory of Molecular Biology (Celgen), University of Leuven, Herestraat 49, B-3000 Leuven, Belgium

EF1 and SIP1 (or Zfhx1a and Zfhx1b, respectively) are the only known members of the vertebrate Zfh1 family of homeodomain/zinc finger-containing proteins. Similar to other transcription factors, both Smad-interacting protein-1 (SIP1) and EF1 are capable of repressing E-cadherin transcription through binding to the E2 boxes located in its promoter. In the case of EF1, this repression has been proposed to occur via interaction with the corepressor C-terminal binding protein (CtBP). In this study, we show by coimmunoprecipitation that SIP1 and CtBP interact in vivo and that an isolated CtBP-binding SIP1 fragment depends on CtBP for transcriptional repression. However, and most importantly, full-length SIP1 and EF1 proteins do not depend on their interaction with CtBP to repress transcription from the E-cadherin promoter. Furthermore, in E-cadherin-positive kidney epithelial cells, the conditional synthesis of mutant SIP1 that cannot bind to CtBP abrogates endogenous E-cadherin expression in a similar way as wild-type SIP1. Our results indicate that full-length SIP1 can repress E-cadherin in a CtBP-independent manner.

Received for publication, January 20, 2003 , and in revised form, April 17, 2003.

^* This work was supported by VIB7 (to D. H.), the University of Leuven Grant OT/00/41 (to D. H.), the Fund for Scientific Research-Flanders Grants G.0243.01 and G.0105.02 (to D. H.), a post-doctoral fellowship (to L. v. G.), the Belgian Federation against Cancer Grant I.23a.2000.F-4 (to K. V.), Fortis Bank (to K. V.), and a post-doctoral fellowship (to G. W.) from the Flemish Institute for Promotion of Industrial Research and Technology Transfer (IWT). 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.

To whom correspondence should be addressed: Dept. of Developmental Biology (VIB7), Flanders Interuniversity Institute for Biotechnology (VIB) and Laboratory of Molecular Biology (Celgen), University of Leuven, Campus Gasthuisberg (Bldg. O&N), Herestraat 49, B-3000 Leuven, Belgium. Tel.: 32-16-34-59-17; Fax: 32-16-34-59-33; E-mail: Kristin.Verschueren{at}med.kuleuven.ac.be.

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