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Papers In Press, published online ahead of print May 1, 2002
J. Biol. Chem, 10.1074/jbc.M201171200
Submitted on February 5, 2002
Revised on March 26, 2002
Accepted on May 1, 2002
Cardiovascular Institute, University of Pittsburgh, Pittsburgh, PA 15213
Corresponding Author: stewartaf{at}msx.upmc.edu
1-Adrenergic-signaling in cardiac myocytes activates the skeletal muscle -actin gene through an MCAT cis-element, the binding site of the 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, and 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.
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