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J. Biol. Chem., Vol. 279, Issue 47, 48930-48940, November 19, 2004
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**
From the
Departments of Cancer Biology, ¶Molecular Physiology and Biophysics, and ||Biochemistry, Vanderbilt University Medical Center, Nashville, Tennessee 37232
Although a number of target genes for the tumor suppressor p53 have been described, the mechanism of p53-dependent apoptosis is incompletely understood. Thus, it is essential to identify and characterize additional target genes that could mediate apoptosis. In the study reported here, we isolated a p53-regulated gene named NDRG1 (N-Myc down-regulated gene 1). Its expression is induced by DNA damage in a p53-dependent fashion. The promoter region of the NDRG1 gene contains a p53 binding site that confers p53-dependent transcriptional activation via a heterologous reporter. RNA interference and inducible gene expression approaches suggest that NDRG1 is necessary but not sufficient for p53-mediated caspase activation and apoptosis. This report further supports the notion that p53 controls a network of genes that are required for its apoptotic function.
Received for publication, January 14, 2004 , and in revised form, August 20, 2004.
* This work was supported in part by National Institutes of Health Grants CA76960 and CA105024 (to P. L.) and Deutsche Akademie der Naturforscher Leopoldina (Germany) Grant BMBF-LPD 9901/8-49 (to S. 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.
Present address: Inst. for Biomedical Research, Georg-Speyer-Haus, Frankfurt/Main, Germany. E-mail: S.Stein{at}med.uni-frankfurt.de.
** To whom correspondence should be addressed. Tel.: 615-936-2182; Fax: 615-936-2183; E-mail: peng.liang{at}vanderbilt.edu.
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