ArticleMolecular and cellular biology1997
Transcription enhancer factor 1 interacts with a basic helix-loop-helix zipper protein, Max, for positive regulation of cardiac alpha-myosin heavy-chain gene expression.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 79 citations in OpenAlex.
- TEAD transcription factor family emerges as a promising therapeutic target for oral squamous cell carcinoma.Frontiers in immunology · 2024Review
- Regulation of the Hippo Pathway Transcription Factor TEAD.Trends in biochemical sciences · 2017Review
- Tead1 is required for maintaining adult cardiomyocyte function, and its loss results in lethal dilated cardiomyopathy.JCI insight · 2017Article
- Global phosphoproteomic profiling reveals perturbed signaling in a mouse model of dilated cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Review
- Tead and AP1 Coordinate Transcription and Motility.Cell reports · 2016Article
- A TEAD1/p65 complex regulates the eutherian-conserved MnSOD intronic enhancer, eRNA transcription and the innate immune response.Biochimica et biophysica acta · 2014Article
- The transcription factor TEAD1 represses smooth muscle-specific gene expression by abolishing myocardin function.The Journal of biological chemistry · 2014Article
- Prognostic value of a nine-gene signature in glioma patients based on mRNA expression profiling.CNS neuroscience & therapeutics · 2014Article
- Structural and functional analysis of the related transcriptional enhancer factor-1 and NF-κB interaction.American journal of physiology. Heart and circulatory physiology · 2014Article
- Article
- Members of the TEAD family of transcription factors regulate the expression of Myf5 in ventral somitic compartments.Developmental biology · 2011Article
- The role of transcription enhancer factors in cardiovascular biology.Trends in cardiovascular medicine · 2011Review
- Alternative requirements for Vestigial, Scalloped, and Dmef2 during muscle differentiation in Drosophila melanogaster.Molecular biology of the cell · 2009Article
- TEAD1 and c-Cbl are novel prostate basal cell markers that correlate with poor clinical outcome in prostate cancer.British journal of cancer · 2008Article
- The cellular antiviral protein viperin is attenuated by proteasome-mediated protein degradation in Japanese encephalitis virus-infected cells.Journal of virology · 2008Article
- Redundant roles of Tead1 and Tead2 in notochord development and the regulation of cell proliferation and survival.Molecular and cellular biology · 2008Article
- HDAC4 and PCAF bind to cardiac sarcomeres and play a role in regulating myofilament contractile activity.The Journal of biological chemistry · 2008Article
- Factors controlling cardiac myosin-isoform shift during hypertrophy and heart failure.Journal of molecular and cellular cardiology · 2007Review
- Insights into transcription enhancer factor 1 (TEF-1) activity from the solution structure of the TEA domain.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
The M-CAT binding factor transcription enhancer factor 1 (TEF-1) has been implicated in the regulation of several cardiac and skeletal muscle genes. Previously, we identified an E-box-M-CAT hybrid (EM) motif that is responsible for the basal and cyclic AMP-inducible expression of the rat cardiac alpha-myosin heavy chain (alpha-MHC) gene in cardiac myocytes. In this study, we report that two factors, TEF-1 and a basic helix-loop-helix leucine zipper protein, Max, bind to the alpha-MHC EM motif. We also found that Max was a part of the cardiac troponin T M-CAT-TEF-1 complex even when the DNA template did not contain an apparent E-box binding site. In the protein-protein interaction assay, a stable association of Max with TEF-1 was observed when glutathione S-transferase (GST)-TEF-1 or GST-Max was used to pull down in vitro-translated Max or TEF-1, respectively. In addition, Max was coimmunoprecipitated with TEF-1, thus documenting an in vivo TEF-1-Max interaction. In the transient transcription assay, overexpression of either Max or TEF-1 resulted a mild activation of the alpha-MHC-chloramphenicol acetyltransferase (CAT) reporter gene at lower concentrations and repression of this gene at higher concentrations. However, when Max and TEF-1 expression plasmids were transfected together, the repression mediated by a single expression plasmid was alleviated and a three- to fourfold transactivation of the alpha-MHC-CAT reporter gene was observed. This effect was abolished once the EM motif in the promoter-reporter construct was mutated, thus suggesting that the synergistic transactivation function of the TEF-1-Max heterotypic complex is mediated through binding of the complex to the EM motif. These results demonstrate a novel association between Max and TEF-1 and indicate a positive cooperation between these two factors in alpha-MHC gene regulation.
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