Mouse DTEF-1 (ETFR-1, TEF-5) Is a Transcriptional Activator in α1-Adrenergic Agonist-stimulated Cardiac Myocytes
| Autor: | Joseph R. Mazzulli, Iain K. Farrance, Tomoji Maeda, Alexandre F. R. Stewart |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
medicine.medical_specialty
Molecular Sequence Data Phosphatase Stimulation Biology Transfection Biochemistry Mice Receptors Adrenergic alpha-1 Internal medicine medicine Animals Myocyte Amino Acid Sequence Adrenergic agonist Promoter Regions Genetic Molecular Biology Transcription factor Cells Cultured DNA Primers Cell Nucleus Base Sequence Sequence Homology Amino Acid Myocardium Cardiac muscle TEA Domain Transcription Factors Skeletal muscle Heart Cell Biology Actins Recombinant Proteins Rats DNA-Binding Proteins Endocrinology medicine.anatomical_structure Animals Newborn embryonic structures Mutagenesis Site-Directed Trans-Activators Phosphorylation Adrenergic alpha-Agonists Sequence Alignment Transcription Factors |
| Zdroj: | Journal of Biological Chemistry. 277:24346-24352 |
| ISSN: | 0021-9258 |
| DOI: | 10.1074/jbc.m201171200 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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