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J. Biol. Chem., Vol. 275, Issue 22, 16865-16870, June 2, 2000
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From the Department of Medical Biochemistry, Ohio State
Neurobiotechnology Center and the Ohio State Biochemistry Program, Ohio
State University, Columbus, Ohio 43210
Previously, we demonstrated that ATF3
(activating transcription
factor-3) is a stress-inducible gene, and the
protein it encodes is a transcriptional repressor. In this report, we
present evidence suggesting that ATF3 represses the transcription of
its own gene. Interestingly, efficient repression requires a consensus
ATF/cAMP-responsive element site in the promoter and a previously
unidentified ATF3-binding site immediately downstream from the TATA
box. Although this new site resembles the known ATF/cAMP-responsive
element sequences at the flanking sequence, it differs from them at the
center key residues. These observations indicate that ATF3 can tolerate
variations in the center of the binding sites if the flanking sequences
are favorable. The repression of the ATF3 promoter by its
own gene product provides a mechanistic explanation, at least in part, for the transient expression pattern of the ATF3 gene upon
stress induction.
Transcriptional Autorepression of the Stress-inducible Gene
ATF3*
,
*
This work was supported by National Institutes of Health
Grant RO1 ES08690 and a grant from the Ohio Cancer Research Associates (to T. H.), by an Ohio State University presidential fellowship and
National Institutes of Health Training Grant T32GM 08512-03 (to
C. D. W.), and by an Ohio State University postdoctoral fellowship (to Y. O.).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.
Present address: NCI, National Institutes of Health, 37 Convent
Dr., MSC4255, Bldg. 37, Bethesda, MD 20892-4255.
§
Present address: Dept. of Molecular Genetics, University of Texas
Southwestern Medical Center, Dallas, TX 75235-9046.
¶
To whom correspondence should be addressed: Neurobiotechnology
Center, Rightmire Hall, Rm. 174, Ohio State University, 1060 Carmack
Rd., Columbus, OH 43210. Tel.: 614-292-2910; Fax: 614-292-5379; E-mail:
hai.2@osu.edu.
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