ReviewWIREs mechanisms of disease
An update on the roles of transcription factor Ets1 in autoimmune diseases.
Review in WIREs mechanisms of disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- The Genomics/Genetics of Primary Biliary Cholangitis: The Case for a Functional SNP rs10893900 in ETS1/FLI1 and Review of the Literature.Clinical reviews in allergy & immunology · 2025Pooled it
- The Roles of Transcription Factor Ets-1 in Neurological Disorders.Molecular neurobiology · 2026Review
- Single-allele chromatin tracing reveals cytokine-dependent super-enhancer repositioning in CD4Immunity · 2026Article
- Single-cell multi-omics dissects transcript isoform and immune repertoire dynamics in human immunosenescence.Science China. Life sciences · 2026Article
- Multiancestry genome-wide association and multiomics analyses elucidate spatiocellular features of multiple sclerosis genetics.Nature genetics · 2026Article
- Integrated Host Genetics and Skin Microbiome Profiling Suggest an HLA-C-Peptostreptococcus Axis in Psoriasis.International journal of molecular sciences · 2026Article
- Refining sequence-to-expression modelling with chromatin accessibility.Bioinformatics (Oxford, England) · 2026Article
- IL-22/IL-22R signaling attenuates mitochondrial damage in PCOS by modulating granulosa cell lipid metabolism through ETS1.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Host Aging Induces a Senescent-Like Phenotype in Neutrophils and Altered Transcriptional Responses to Streptococcus pneumoniae.Aging cell · 2026Article
- HLA class I-naturally presented synovial tissue peptides are recognized by CD8+ T lymphocytes from rheumatoid arthritis patients.Frontiers in immunology · 2026Article
- Elucidate senescence-related gene signature and immune infiltration landscape in abdominal aortic aneurysm.PloS one · 2026Article
- Fatty acid synthesis promotes mtDNA release via ETS1-mediated oligomerization of VDAC1 facilitating endothelial dysfunction in sepsis-induced lung injury.Cell death and differentiation · 2025Article
- Spatial proteomics and transcriptomics reveal early immune cell organization in pancreatic intraepithelial neoplasia.JCI insight · 2025Article
- B cell development: transcriptional regulation and immunological mechanisms in homeostasis.Frontiers in immunology · 2025Review
- Cellular Senescence Genes as Cutting-Edge Signatures for Abdominal Aortic Aneurysm Diagnosis: Potential for Innovative Therapeutic Interventions.Journal of cellular and molecular medicine · 2025Article
- Investigation in the cannabigerol derivative VCE-003.2 as a disease-modifying agent in a mouse model of experimental synucleinopathy.Behavioral and brain functions : BBF · 2024Article
- From molecular subgroups to molecular targeted therapy in rheumatoid arthritis: A bioinformatics approach.Heliyon · 2024Article
- ETS1 Function in Leukemia and Lymphoma.Advances in experimental medicine and biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Transcription factors are crucial to regulate gene expression in immune cells and in other cell types. In lymphocytes, there are a large number of different transcription factors that are known to contribute to cell differentiation and the balance between quiescence and activation. One such transcription factor is E26 oncogene homolog 1 (Ets1). Ets1 expression is high in quiescent B and T lymphocytes and its levels are decreased upon activation. The human ETS1 gene has been identified as a susceptibility locus for many autoimmune and inflammatory diseases. In accord with this, gene knockout of Ets1 in mice leads to development of a lupus-like autoimmune disease, with enhanced activation and differentiation of both B cells and T cells. Prior reviews have summarized functional roles for Ets1 based on studies of Ets1 knockout mice. In recent years, numerous additional studies have been published that further validate ETS1 as a susceptibility locus for human diseases where immune dysregulation plays a causative role. In this update, new information that further links Ets1 to human autoimmune diseases is organized and collated to serve as a resource. This update also describes recent studies that seek to understand molecularly how Ets1 regulates immune cell activation, either using human cells and tissues or mouse models. This resource is expected to be useful to investigators seeking to understand how Ets1 may regulate the human immune response, particularly in terms of its roles in autoimmunity and inflammation. This article is categorized under: Immune System Diseases > Genetics/Genomics/Epigenetics Immune System Diseases > Molecular and Cellular Physiology.
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What Socratic holds
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 Socratic graph.