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J. Biol. Chem., Vol. 276, Issue 1, 298-305, January 5, 2001
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From the Program in Molecular Biology and Department of Radiation
Oncology, Stritch School of Medicine, Loyola University Medical Center,
Maywood, Illinois 60153
The p53 tumor suppressor protein regulates the
transcription of regulatory genes involved in cell cycle arrest and
apoptosis. We reported previously that overexpression of p202, an
interferon-inducible negative regulator of cell growth, negatively
regulates the transcriptional activity of p53. Now we identify the gene
encoding p202 as one whose mRNA and protein expression decrease in
cells following the expression of wild-type, but not mutant, p53.
Furthermore, the levels of p202 also decrease after exposure of cells
to ultra violet light, which correlate with increase in the levels of
p53. We report that the sequence-specific DNA binding of p53 to the 5'-regulatory region of the 202 gene contributes to
the transcriptional repression of the 202 gene.
Interestingly, overexpression of p202 in cells induced to undergo
p53-dependent apoptosis significantly delays this process,
indicating that the negative regulation of the 202 gene by
wild-type p53 is important to potentiate apoptosis.
The Gene Encoding p202, an Interferon-inducible Negative
Regulator of the p53 Tumor Suppressor, Is a Target of p53-mediated
Transcriptional Repression*
*
This work was supported by National Institutes of Health
Grant CA69031.The costs of publication of this
article were defrayed in part by the
payment of page charges. The 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 Radiation
Oncology, Stritch School of Medicine, Loyola University Medical Center,
2160 S. First Ave., Bldg. 1, Maywood, IL 60153. Tel.: 708-202-8387 (ext. 23407); Fax: 708-202-2647; E-mail:
dchoube@rdth2.rdth.luc.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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