ArticleArthritis research & therapy2020
Synergistic activation of NF-κB by TNFAIP3 (A20) reduction and UBE2L3 (UBCH7) augment that synergistically elevate lupus risk.
Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 25 citations in OpenAlex.
- Ivangustin, a sesquiterpene lactone from Inula japonica Thunb., attenuates neuroinflammation through covalent inhibition of ubiquitin-conjugating enzyme UBE2L3.Chinese medicine · 2026Article
- Emerging perspectives in proteostasis: bridging mechanisms and therapeutics for human diseases.Signal transduction and targeted therapy · 2026Review
- OTU deubiquitinases as immune-circuit editors: from human immunopathology to therapeutic prioritization.Frontiers in immunology · 2026Review
- From Reshaped Metabolome to Repaired Skin: FermentedAntioxidants (Basel, Switzerland) · 2025Article
- Ubiquitin-proteasome system: a potential participant and therapeutic target in antiphospholipid syndrome.Frontiers in immunology · 2025Review
- A20 as a Potential Therapeutic Target for COVID-19.Immunity, inflammation and disease · 2025Review
- Investigating the shared genetic basis of inflammatory bowel disease and systemic lupus erythematosus using genetic overlap analysis.BMC genomics · 2024Article
- UBE2L3 expression in human gastric cancer and its clinical significance.Journal of cancer research and clinical oncology · 2024Article
- The Complexity of Being A20: From Biological Functions to Genetic Associations.Journal of clinical immunology · 2024Review
- Attenuation of HOIL-1L ligase activity promotes systemic autoimmune disorders by augmenting linear ubiquitin signaling.JCI insight · 2024Article
- Lupus Nephritis: Current Perspectives and Moving Forward.Journal of inflammation research · 2022Review
- MX2: Identification and systematic mechanistic analysis of a novel immune-related biomarker for systemic lupus erythematosus.Frontiers in immunology · 2022Article
- UBE2L3, a Partner of MuRF1/TRIM63, Is Involved in the Degradation of Myofibrillar Actin and Myosin.Cells · 2021Article
- [Experimental study on the effect of zinc finger protein A20 on lumbar intervertebral disc degeneration in rabbits].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2021Article
- Effects of Upregulation of TNFAIP3 on Diabetic Neuropathic Pain in Mice.Disease markers · 2021Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSystemic lupus erythematosus (SLE) is an autoimmune inflammatory rheumatic disease. SLE susceptibility is affected by multiple genetic elements, environmental factors, and their interactions. We aimed in this study to statistically and functionally characterize a gene-gene interaction (epistasis) recently documented to affect SLE risk.
methodsTwo single-nucleotide polymorphisms, rs2230926 in TNFAIP3 (A20) gene and rs131654 in UBE2L3 (UBCH7) gene, were genotyped in all 3525 Korean participants, and their SLE risk association and epistasis were statistically analyzed by calculating odds ratio (OR), 95% confidence interval (CI), and P values in genotype comparisons between 1318 SLE patients and 2207 healthy controls. Furthermore, their effects on gene functions were assessed by comparatively examining separate and combined effects of TNFAIP3 and UBE2L3 knockdowns on NF-κB transcription factor activity in human cells.
resultsSLE susceptibility is associated with TNFAIP3 rs2230926 (OR = 1.9, 95% CI 1.6-2.4, P = 8.6 × 10
conclusionsA synergistic interaction between TNFAIP3 and UBE2L3 genes is observed in SLE risk, as being evident in comparison of genotype distributions between SLE patients and controls. Additionally, the synergistic gene-gene interaction is functionally validated, as TNFAIP3 reduction and UBE2L3 augment exert synergism in activation of NF-κB and subsequent induction of inflammatory cytokines. Accordingly, SLE inflammation and risk could be synergistically alleviated by TNFAIP3 upregulation and UBE2L3 downregulation.
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