ArticlePloS one2015
EGR1 Functions as a Potent Repressor of MEF2 Transcriptional Activity.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
- Focal Adhesion's Role in Cardiomyocytes Function: From Cardiomyogenesis to Mechanotransduction.Cells · 2024Review
- HDAC5 inhibition attenuates ventricular remodeling and cardiac dysfunction.Orphanet journal of rare diseases · 2023Article
- Genetic distinction between functional tissue-resident and conventional natural killer cells.iScience · 2023Article
- Myocyte Enhancer Factor 2A Plays a Central Role in the Regulatory Networks of Cellular Physiopathology.Aging and disease · 2023Review
- Early fish domestication affects methylation of key genes involved in the rapid onset of the farmed phenotype.Epigenetics · 2022Article
- EGR1 is a gatekeeper of inflammatory enhancers in human macrophages.Science advances · 2021Article
- EGR1 interacts with DNMT3L to inhibit the transcription of miR-195 and plays an anti-apoptotic role in the development of gastric cancer.Journal of cellular and molecular medicine · 2019Article
- A genome-wide interactome of DNA-associated proteins in the human liver.Genome research · 2017Article
- HTLV-1 Tax upregulates early growth response protein 1 through nuclear factor-κB signaling.Oncotarget · 2017Article
- Regulation of early growth response 2 expression by secreted frizzled related protein 1.BMC cancer · 2017Article
- Article
- Transcription factors, coregulators, and epigenetic marks are linearly correlated and highly redundant.PloS one · 2017Article
- The Function of the MEF2 Family of Transcription Factors in Cardiac Development, Cardiogenomics, and Direct Reprogramming.Journal of cardiovascular development and disease · 2016Article
- The progress of early growth response factor 1 and leukemia.Intractable & rare diseases research · 2016Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The myocyte enhancer factor 2 (MEF2) transcription factor requires interactions with co-factors for precise regulation of its target genes. Our lab previously reported that the mammalian MEF2A isoform regulates the cardiomyocyte costamere, a critical muscle-specific focal adhesion complex involved in contractility, through its transcriptional control of genes encoding proteins localized to this cytoskeletal structure. To further dissect the transcriptional mechanisms of costamere gene regulation and identify potential co-regulators of MEF2A, a bioinformatics analysis of transcription factor binding sites was performed using the proximal promoter regions of selected costamere genes. One of these predicted sites belongs to the early growth response (EGR) transcription factor family. The EGR1 isoform has been shown to be involved in a number of pathways in cardiovascular homeostasis and disease, making it an intriguing candidate MEF2 coregulator to further characterize. Here, we demonstrate that EGR1 interacts with MEF2A and is a potent and specific repressor of MEF2 transcriptional activity. Furthermore, we show that costamere gene expression in cardiomyocytes is dependent on EGR1 transcriptional activity. This study identifies a mechanism by which MEF2 activity can be modulated to ensure that costamere gene expression is maintained at levels commensurate with cardiomyocyte contractile activity.
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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.