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J. Biol. Chem., Vol. 278, Issue 35, 32899-32904, August 29, 2003

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Regulation of Proglucagon Transcription by Activated Transcription Factor (ATF) 3 and a Novel Isoform, ATF3b, through the cAMP-response Element/ATF Site of the Proglucagon Gene Promoter^*

Jie Wang , Yun Cao  and Donald F. Steiner   ¶

From the Department of Biochemistry and Molecular Biology and the Howard Hughes Medical Institute, University of Chicago, Chicago, Illinois 60637

Glucagon, the second major glucose-regulated hormone in the control of glucose homeostasis, functions as a counter-regulator to insulin and is specifically produced by the pancreatic cells. Its excessive biosynthesis and secretion is associated with diabetes mellitus. The expression of the proglucagon gene has been demonstrated to be regulated by a cAMP-dependent pathway through cAMP-response element-binding protein (CREB) and possibly other transcription factors bound to its cAMP-response element (CRE)/activated transcription factor (ATF) site. Elsewhere we have shown that ATF3, a member of the ATF/CREB subfamily of the basic leucine zipper domain proteins, is expressed predominantly in the cells of the pancreatic islets. In our attempts to further dissect the role of ATF3 proteins in cells, we have identified and characterized a novel alternatively spliced form, ATF3b, and have compared the specific binding ability of ATF3 and ATF3b on the CRE/ATF motif of the proglucagon promoter. Our findings indicate the existence of a novel mechanism by which the transcription of the proglucagon gene is regulated in response to cAMP signals, in addition to CREB and in relation to glucose fluctuations in pancreatic cells.

Received for publication, May 23, 2003 , and in revised form, June 16, 2003.

The nucleotide sequence(s) reported in this paper has been submitted to the DDBJ/GenBank^TM/EBI Data Bank with accession number(s) AY329367.

^* This work was supported by National Institutes of Health Grants DK13914 and DK20595 and by the Howard Hughes Medical Institute. 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: The Howard Hughes Medical Institute, University of Chicago, 5841 S. Maryland Ave., MC 1028, Rm. 216, Chicago, IL 60637. Tel.: 773-702-1334; Fax: 773-702-4292; E-mail: dfsteine{at}midway.uchicago.edu.

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