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Originally published In Press as doi:10.1074/jbc.M201171200 on May 1, 2002

J. Biol. Chem., Vol. 277, Issue 27, 24346-24352, July 5, 2002
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Mouse DTEF-1 (ETFR-1, TEF-5) Is a Transcriptional Activator in alpha 1-Adrenergic Agonist-stimulated Cardiac Myocytes*

Tomoji MaedaDagger , Joseph R. MazzulliDagger , Iain K. G. Farrance§, and Alexandre F. R. StewartDagger ||

From the Dagger  Cardiovascular Institute, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15213 and the § Department of Biochemistry and Molecular Biology, University of Maryland, Baltimore, Maryland 21201

alpha 1-Adrenergic signaling in cardiac myocytes activates the skeletal muscle alpha -actin gene through an MCAT cis-element, the binding site of the transcriptional enhancer factor-1 (TEF-1) family of transcription factors. TEF-1 accounts for more than 85% of the MCAT binding activity in neonatal rat cardiac myocytes. Other TEF-1 family members account for the rest. Although TEF-1 itself has little effect on the alpha 1-adrenergic activation of skeletal muscle alpha -actin, the related factor RTEF-1 augments the response and is a target of alpha 1-adrenergic signaling. Here, we examined another TEF-1 family member expressed in cardiac muscle, DTEF-1, and observed that it also augmented the alpha 1-adrenergic response of skeletal muscle alpha -actin. A DTEF-1 peptide-specific antibody revealed that endogenous DTEF-1 accounts for up to 5% of the MCAT binding activity in neonatal rat cardiac myocytes. A TEF-1/DTEF-1 chimera suggests that alpha 1-adrenergic signaling modulates DTEF-1 function. Orthophosphate labeling and immunoprecipitation of an epitope-tagged DTEF-1 showed that DTEF-1 is phosphorylated in vivo. alpha 1-Adrenergic stimulation increased while phosphatase treatment lowered the MCAT binding by DTEF-1 and the endogenous non-TEF-1 MCAT-binding factor. In contrast, alpha 1-adrenergic stimulation did not alter, and phosphatase treatment increased, MCAT binding of TEF-1 and RTEF-1. Taken together, these results suggest that DTEF-1 is a target for alpha 1-adrenergic activation of the skeletal muscle alpha -actin gene in neonatal rat cardiac myocytes.

* 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.

Supported by Grant P01 HL27867 from the National Institutes of Health.

|| Supported by a Grant-in-aid from the American Heart Association (0050282N) and by Grant R29 HL57211 from the National Institutes of Health. To whom correspondence should be addressed: Cardiovascular Inst., School of Medicine, University of Pittsburgh, BST 1704.3, 200 Lothrop St., Pittsburgh, PA 15213. Tel.: 412-383-9761; Fax: 412-383-8997; E-mail: stewartaf@msx.upmc.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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