ArticleNature genetics2018
Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity.
Article in Nature genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers, 1 of them a synthesis that pooled it.
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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
236 citing papers in PubMed, 1 synthesis or guideline pooled it, 407 citations in OpenAlex.
- Trans-eQTL mapping prioritises USP18 as a negative regulator of interferon response at a lupus risk locus.Nature communications · 2025Pooled it
- The case for an Epstein-Barr virus vaccine: Lessons from its link to systemic lupus erythematosus.Human vaccines & immunotherapeutics · 2026Review
- A highly prevalent lupus risk haplotype increases IRF7-dependent induction of IFN-α, enhancing antiviral defense and exacerbating autoimmunity.American journal of human genetics · 2026Article
- Functional characterization of viral transcriptional regulators reveals extensive rewiring of host pathways.Nature communications · 2026Article
- Machine learning models identify prognostic factors in systemic lupus erythematosus patients with epstein-barr virus infection.Clinical rheumatology · 2026Article
- Epigenetic regulation of B cell tolerance and dysfunction in autoimmune disease.Nature reviews. Immunology · 2026Review
- Article
- Systematic investigation reveals extensive Epstein-Barr virus transcriptional regulation of the human genome.Cell genomics · 2026Article
- Multitrait analysis of genome-wide association studies expands eosinophilic esophagitis genetic susceptibility and polygenic risk scores.The Journal of allergy and clinical immunology · 2026Article
- High-resolution promoter interaction analysis implicates genes involved in activation of type 3 innate lymphoid cells in immune disease risk.Nature genetics · 2026Article
- Autoimmune non-coding variants perturb transcription factor-cofactor complex assembly linked to enhancer activity.bioRxiv : the preprint server for biology · 2026Article
- From Genes to Pathways: The Molecular Landscape of Systemic Lupus Erythematosus.International journal of molecular sciences · 2026Review
- Neuroinflammation as a result of non-neurotropic herpesvirus infection.Immunology and cell biology · 2026Review
- Why Is MS a More Frequent Complication of EBV Infection in Females?Immunological reviews · 2026Review
- Article
- A CRISPR-Cas9 screen Reveals STEEP1 as a Key Host Dependency Factor for Epstein-Barr Virus Latent Membrane Protein 1 Trafficking and Signaling.bioRxiv : the preprint server for biology · 2026Article
- Gene regulatory network determinants of rapid recall in human memory CD4Cell reports · 2026Article
- Identifying genetic and cellular connections and distinctions among 15 autoimmune diseases using an in-silico approach.Communications medicine · 2026Article
- Elevated levels of advanced glycation end-products AGE10 in patients with reactive arthritis caused by Chlamydia trachomatis and Epstein-Barr virus infection.Immunologic research · 2026Article
- Memory T cell rapid recall is driven by memory-specific AP-1 recruitment determined by epigenome and co-factor interactions.bioRxiv : the preprint server for biology · 2026Article
176 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Explaining the genetics of many diseases is challenging because most associations localize to incompletely characterized regulatory regions. Using new computational methods, we show that transcription factors (TFs) occupy multiple loci associated with individual complex genetic disorders. Application to 213 phenotypes and 1,544 TF binding datasets identified 2,264 relationships between hundreds of TFs and 94 phenotypes, including androgen receptor in prostate cancer and GATA3 in breast cancer. Strikingly, nearly half of systemic lupus erythematosus risk loci are occupied by the Epstein-Barr virus EBNA2 protein and many coclustering human TFs, showing gene-environment interaction. Similar EBNA2-anchored associations exist in multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, juvenile idiopathic arthritis and celiac disease. Instances of allele-dependent DNA binding and downstream effects on gene expression at plausibly causal variants support genetic mechanisms dependent on EBNA2. Our results nominate mechanisms that operate across risk loci within disease phenotypes, suggesting new models for disease origins.
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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.