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J. Biol. Chem., Vol. 277, Issue 27, 24346-24352, July 5, 2002
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From the
Mouse DTEF-1 (ETFR-1, TEF-5) Is a Transcriptional Activator
in
1-Adrenergic Agonist-stimulated Cardiac
Myocytes*
,,
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
1-Adrenergic signaling in
cardiac myocytes activates the skeletal muscle -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
1-adrenergic activation of skeletal muscle -actin,
the related factor RTEF-1 augments the response and is a target of
1-adrenergic signaling. Here, we examined another TEF-1
family member expressed in cardiac muscle, DTEF-1, and observed that it
also augmented the 1-adrenergic response of skeletal
muscle -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
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.
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, 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 1-adrenergic
activation of the skeletal muscle -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 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.
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