ArticleNature communications2018
Dissection and function of autoimmunity-associated TNFAIP3 (A20) gene enhancers in humanized mouse models.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
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- Delivering miR-23b-3p by small extracellular vesicles to promote cell senescence and aberrant lipid metabolism.BMC biology · 2025Article
- CRISPR-Cas9 editing ofFrontiers in genome editing · 2025Article
- Therapeutic CRISPR epigenome editing of inflammatory receptors in the intervertebral disc.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Systemic lupus erythematosus genetics: insights into pathogenesis and implications for therapy.Nature reviews. Rheumatology · 2024Review
- 3D genome organization and epigenetic regulation in autoimmune diseases.Frontiers in immunology · 2023Review
- TGFβ reprograms TNF stimulation of macrophages towards a non-canonical pathway driving inflammatory osteoclastogenesis.Nature communications · 2022Article
- The Intersection of Cellular and Systemic Metabolism: Metabolic Syndrome in Systemic Lupus Erythematosus.Endocrinology · 2022Review
- A CD40 variant is associated with systemic bone loss among patients with rheumatoid arthritis.Clinical rheumatology · 2022Article
- Systemic lupus erythematosus variants modulate the function of an enhancer upstream ofFrontiers in genetics · 2022Article
- MiR-342 controls Mycobacterium tuberculosis susceptibility by modulating inflammation and cell death.EMBO reports · 2021Article
- Construction and analysis for dys-regulated lncRNAs and mRNAs in LPS-induced porcine PBMCs.Innate immunity · 2021Article
- A20: a master regulator of arthritis.Arthritis research & therapy · 2020Review
- Two distinct ubiquitin-binding motifs in A20 mediate its anti-inflammatory and cell-protective activities.Nature immunology · 2020Article
- Prioritizing disease and trait causal variants at the TNFAIP3 locus using functional and genomic features.Nature communications · 2020Article
- Regulatory network mediated by RBP-J/NFATc1-miR182 controls inflammatory bone resorption.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- A20 at the Crossroads of Cell Death, Inflammation, and Autoimmunity.Cold Spring Harbor perspectives in biology · 2020Review
- TNFAIP3 Plays a Role in Aging of the Hematopoietic System.Frontiers in immunology · 2020Article
- Genetic variations in A20 DUB domain provide a genetic link to citrullination and neutrophil extracellular traps in systemic lupus erythematosus.Annals of the rheumatic diseases · 2019Article
- TNF-induced inflammatory genes escape repression in fibroblast-like synoviocytes: transcriptomic and epigenomic analysis.Annals of the rheumatic diseases · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Enhancers regulate gene expression and have been linked with disease pathogenesis. Little is known about enhancers that regulate human disease-associated genes in primary cells relevant for pathogenesis. Here we use BAC transgenics and genome editing to dissect, in vivo and in primary immune cells, enhancers that regulate human TNFAIP3, which encodes A20 and is linked with autoimmune diseases. A20 expression is dependent on a topologically associating subdomain (sub-TAD) that harbors four enhancers, while another >20 enhancers in the A20 locus are redundant. This sub-TAD contains cell- and activation-specific enhancers, including an enhancer (termed TT>A) harboring a proposed causal SLE-associated SNV. Deletion of the sub-TAD or the TT>A enhancer results in enhanced inflammatory responses, autoantibody production, and inflammatory arthritis, thus establishing functional importance in vivo and linking enhancers with a specific disease phenotype. These findings provide insights into enhancers that regulate human A20 expression to prevent inflammatory pathology and autoimmunity.
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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.