ArticleThe Journal of biological chemistry2012
The transcription factor Erg controls endothelial cell quiescence by repressing activity of nuclear factor (NF)-κB p65.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- ERG preserves endothelial identity to limit atherosclerosis.Nature communications · 2026Article
- From brown to white: Brown adipose tissue endothelial cells whiten in culture conditions.Molecular metabolism · 2026Article
- ERG-deficient endothelium identifies IL-8/CXCR2 axis as a therapeutic target for resolving neutrophilic lung vascular injury.JCI insight · 2026Article
- Dynamic activity of Erg promotes maturation of the hematopoietic system.Blood advances · 2026Article
- Obesity drives depot-specific vascular remodeling in male white adipose tissue.Nature communications · 2025Article
- High Shear Stress Reduces ERG Causing Endothelial-Mesenchymal Transition and Pulmonary Arterial Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Case Report: A heterozygous loss-of-function variant of theFrontiers in cardiovascular medicine · 2025Article
- Transcription factor networks in cellular quiescence.Nature cell biology · 2025Review
- Stiffness-induced modulation of ERG transcription factor in chronic liver disease.Npj gut and liver · 2024Article
- Oxidative Stress Induces E-Selectin Expression through Repression of Endothelial Transcription Factor ERG.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- NF-κB/p52 augments ETS1 binding genome-wide to promote glioma progression.Communications biology · 2023Article
- Review
- Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis.Nature cardiovascular research · 2022Article
- Endothelial Cell Metabolism in Vascular Functions.Cancers · 2022Review
- Review
- Emerging roles of inflammation-mediated endothelial-mesenchymal transition in health and disease.Inflammation and regeneration · 2022Review
- Leveraging cell-type-specific regulatory networks to interpret genetic variants in abdominal aortic aneurysm.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Evaluating whole-genome expression differences in idiopathic and diabetic adhesive capsulitis.Journal of shoulder and elbow surgery · 2022Article
- MicroRNA negatively regulates NF-κB-mediated immune responses by targeting NOD1 in the teleost fish Miichthys miiuy.Science China. Life sciences · 2021Article
- A non-coding genetic variant associated with abdominal aortic aneurysm alters ERG gene regulation.Human molecular genetics · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
The interaction of transcription factors with specific DNA sequences is critical for activation of gene expression programs. In endothelial cells (EC), the transcription factor NF-κB is important in the switch from quiescence to activation, and is tightly controlled to avoid excessive inflammation and organ damage. Here we describe a novel mechanism that controls the activation of NF-κB in EC. The transcription factor Erg, the most highly expressed ETS member in resting EC, controls quiescence by repressing proinflammatory gene expression. Focusing on intercellular adhesion molecule 1(ICAM)-1 as a model, we identify two ETS binding sites (EBS -118 and -181) within the ICAM-1 promoter required for Erg-mediated repression. We show that Erg binds to both EBS -118 and EBS -181, the latter located within the NF-κB binding site. Interestingly, inhibition of Erg expression in quiescent EC results in increased NF-κB-dependent ICAM-1 expression, indicating that Erg represses basal NF-κB activity. Erg prevents NF-κB p65 from binding to the ICAM-1 promoter, suggesting a direct mechanism of interference. Gene set enrichment analysis of transcriptome profiles of Erg and NF-κB-dependent genes, together with chromatin immunoprecipitation (ChIP) studies, reveals that this mechanism is common to other proinflammatory genes, including cIAP-2 and IL-8. These results identify a role for Erg as a gatekeeper controlling vascular inflammation, thus providing an important barrier to protect against inappropriate endothelial activation.
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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.