Mouse DTEF-1 (ETFR-1, TEF-5) is a transcriptional activator in α1-adrenergic agonist-stimulated cardiac myocytes

Tomoji Maeda, Joseph R. Mazzulli, Iain K G Farrance, Alexandre F R Stewart

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

α1-Adrenergic signaling in cardiac myocytes activates the skeletal muscle a-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 α1-adrenergic activation of skeletal muscle α-actin, the related factor RTEF-1 augments the response and is a target of α1-adrenergic signaling. Here, we examined another TEF-1 family member expressed in cardiac muscle, DTEF-1, and observed that it also augmented the α1-adrenergic response of skeletal muscle α-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 α1-adrenergic signaling modulates DTEF-1 function. Orthophosphate labeling and immunoprecipitation of an epitope-tagged DTEF-1 showed that DTEF-1 is phosphorylated in vivo. α1-Adrenergic stimulation increased while phosphatase treatment lowered the MCAT binding by DTEF-1 and the endogenous non-TEF-1 MCAT-binding factor. In contrast, α1-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 α1-adrenergic activation of the skeletal muscle α-actin gene in neonatal rat cardiac myocytes.

Original languageEnglish (US)
Pages (from-to)24346-24352
Number of pages7
JournalJournal of Biological Chemistry
Volume277
Issue number27
DOIs
StatePublished - Jul 5 2002

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Adrenergic Agonists
Cardiac Myocytes
Adrenergic Agents
Muscle
Actins
Skeletal Muscle
Rats
Phosphoric Monoester Hydrolases
Genes
Chemical activation
Immunoprecipitation
Labeling
5-(4-hydroxy-3-methoxyphenyl)-5-phenylhydantoin
Epitopes
Myocardium
Transcription Factors
Phosphates
Binding Sites
Peptides
Antibodies

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Maeda, Tomoji ; Mazzulli, Joseph R. ; Farrance, Iain K G ; Stewart, Alexandre F R. / Mouse DTEF-1 (ETFR-1, TEF-5) is a transcriptional activator in α1-adrenergic agonist-stimulated cardiac myocytes. In: Journal of Biological Chemistry. 2002 ; Vol. 277, No. 27. pp. 24346-24352.
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abstract = "α1-Adrenergic signaling in cardiac myocytes activates the skeletal muscle a-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 α1-adrenergic activation of skeletal muscle α-actin, the related factor RTEF-1 augments the response and is a target of α1-adrenergic signaling. Here, we examined another TEF-1 family member expressed in cardiac muscle, DTEF-1, and observed that it also augmented the α1-adrenergic response of skeletal muscle α-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 α1-adrenergic signaling modulates DTEF-1 function. Orthophosphate labeling and immunoprecipitation of an epitope-tagged DTEF-1 showed that DTEF-1 is phosphorylated in vivo. α1-Adrenergic stimulation increased while phosphatase treatment lowered the MCAT binding by DTEF-1 and the endogenous non-TEF-1 MCAT-binding factor. In contrast, α1-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 α1-adrenergic activation of the skeletal muscle α-actin gene in neonatal rat cardiac myocytes.",
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Mouse DTEF-1 (ETFR-1, TEF-5) is a transcriptional activator in α1-adrenergic agonist-stimulated cardiac myocytes. / Maeda, Tomoji; Mazzulli, Joseph R.; Farrance, Iain K G; Stewart, Alexandre F R.

In: Journal of Biological Chemistry, Vol. 277, No. 27, 05.07.2002, p. 24346-24352.

Research output: Contribution to journalArticle

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AU - Maeda, Tomoji

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N2 - α1-Adrenergic signaling in cardiac myocytes activates the skeletal muscle a-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 α1-adrenergic activation of skeletal muscle α-actin, the related factor RTEF-1 augments the response and is a target of α1-adrenergic signaling. Here, we examined another TEF-1 family member expressed in cardiac muscle, DTEF-1, and observed that it also augmented the α1-adrenergic response of skeletal muscle α-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 α1-adrenergic signaling modulates DTEF-1 function. Orthophosphate labeling and immunoprecipitation of an epitope-tagged DTEF-1 showed that DTEF-1 is phosphorylated in vivo. α1-Adrenergic stimulation increased while phosphatase treatment lowered the MCAT binding by DTEF-1 and the endogenous non-TEF-1 MCAT-binding factor. In contrast, α1-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 α1-adrenergic activation of the skeletal muscle α-actin gene in neonatal rat cardiac myocytes.

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