ArticleNucleic acids research2000
Protein kinase-A dependent phosphorylation of transcription enhancer factor-1 represses its DNA-binding activity but enhances its gene activation ability.
Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 50 citations in OpenAlex.
- A-Kinase Anchor Protein 4 (proAKAP4): Protein Molecule-Based Fertility Marker of Indonesian Dairy Bull and Its Correlation With Frozen-Thawed Sperm Quality.Veterinary medicine international · 2025Article
- The RNF214-TEAD-YAP signaling axis promotes hepatocellular carcinoma progression via TEAD ubiquitylation.Nature communications · 2024Article
- Design, Synthesis, and Bioevaluation of Transcriptional Enhanced Assocciated Domain (TEAD) PROTAC Degraders.ACS medicinal chemistry letters · 2024Article
- TM7SF3 controls TEAD1 splicing to prevent MASH-induced liver fibrosis.Cell metabolism · 2024Article
- RBFOX2-regulated TEAD1 alternative splicing plays a pivotal role in Hippo-YAP signaling.Nucleic acids research · 2022Article
- Tight junction protein ZO-2 modulates the nuclear accumulation of transcription factor TEAD.Molecular biology of the cell · 2021Article
- Review
- Alternative splicing rewires Hippo signaling pathway in hepatocytes to promote liver regeneration.Nature structural & molecular biology · 2018Article
- Regulation of the Hippo Pathway Transcription Factor TEAD.Trends in biochemical sciences · 2017Review
- Review
- Article
- The TEA transcription factor Tec1 links TOR and MAPK pathways to coordinate yeast development.Genetics · 2011Article
- Alternative requirements for Vestigial, Scalloped, and Dmef2 during muscle differentiation in Drosophila melanogaster.Molecular biology of the cell · 2009Article
- Factors controlling cardiac myosin-isoform shift during hypertrophy and heart failure.Journal of molecular and cellular cardiology · 2007Review
- Vestigial-like-2b (VITO-1b) and Tead-3a (Tef-5a) expression in zebrafish skeletal muscle, brain and notochord.Gene expression patterns : GEP · 2007Article
- Identification of a new hybrid serum response factor and myocyte enhancer factor 2-binding element in MyoD enhancer required for MyoD expression during myogenesis.Molecular biology of the cell · 2007Article
- 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
- Molecular and functional analysis of scalloped recessive lethal alleles in Drosophila melanogaster.Genetics · 2004Article
- A TEF-1-element is required for activation of the promoter of pseudorabies virus glycoprotein X gene by IE180.Virus genes · 2002Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The cAMP-dependent signaling pathway has been implicated in cardiac cell growth/differentiation and muscle gene transcription. Previously, we have identified a cAMP-inducible E-box/M-CAT hybrid motif in the cardiac alpha-myosin heavy chain (alpha-MHC) gene promoter. The two factors, TEF-1 and Max, that bind to this motif are found to physically associate with each other and exert a positive cooperative effect for gene regulation. Here we show that TEF-1, but not Max, is a substrate for protein kinase-A (PK-A)-dependent phosphorylation. TEF-1 is phosphorylated by PK-A at residue serine-102. This post-translational modification of TEF-1 repressed its DNA-binding activity, but not its ability to interact with the Max protein. Replacement of serine-102 in TEF-1 by a neutral or a charged amino acid did not abolish its DNA-binding ability, suggesting that changing a charge at the 102 amino-acid position of TEF-1 was not sufficient to inhibit its DNA-binding activity. We also show that PK-A response of the alpha-MHC gene is stimulated by the presence of wild-type TEF-1 but not by mutant TEF-1 having serine-102 replaced by alanine, suggesting that phosphorylation at this residue accounts for the cAMP/PK-A response of the gene. Thus, these data demonstrate that TEF-1 is a direct target of cAMP/PK-A signaling in cardiac myocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.