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J. Biol. Chem., Vol. 281, Issue 1, 269-278, January 6, 2006

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Physical Interaction and Mutual Transrepression between CCAAT/Enhancer-binding Protein and the p53 Tumor Suppressor^*

Tanja Schneider-Merck, Yvonne Pohnke, Rita Kempf, Mark Christian¶, Jan J. Brosens¶, and Birgit Gellersen1

From the Endokrinologikum Hamburg, Hamburg 20251, Germany, the Institute for Hormone and Fertility Research, University of Hamburg, Hamburg 20251, Germany, and the ^¶Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Hospital, London W12 ONN, United Kingdom

The tumor suppressor protein p53 is not only involved in defending cells against genotoxic insults but is also implicated in differentiation processes, a function that it shares with the CCAAT/enhancer-binding protein (C/EBP). We previously reported an up-regulation of both factors in the cycle-dependent differentiation process of human endometrial stromal cells, termed decidualization. C/EBP-mediated activation of a decidualization marker, the decidual prolactin promoter, was antagonized by p53. Here we report that C/EBP in turn represses the transcriptional activity of p53. Competition for limiting amounts of coactivator CREB-binding protein/p300 was ruled out as the underlying mechanism of transrepression. Physical interaction between p53 and C/EBP was demonstrated in vitro and in vivo and shown to depend on the C-terminal domains of both proteins. In gel shift experiments, C/EBP reduced complex formation between p53 and its response element. Conversely, p53 strongly inhibited binding of endogenous C/EBP from endometrial stromal cells to the C/EBP-responsive region in the decidual prolactin promoter. The observed negative cross-talk between p53 and C/EBP is likely to impact expression of their respective target genes.

Received for publication, March 30, 2005 , and in revised form, October 4, 2005.

^* This work was supported by Deutsche Forschungsgemeinschaft Grant Ge 748/9-1/9-2 (to B. G.), Wellcome Trust Clinical Scientist Fellowship 54043 (to J. J. B.), and a Royal Society Joint Project Grant. 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.

¹ To whom correspondence should be addressed: Endokrinologikum Hamburg, Falkenried 88, Hamburg 20251, Germany. Tel.: 49-40-471965-91; Fax: 49-40-471965-99; E-mail: gellersen{at}endokrinologikum.com.

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