{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T16:12:23Z","timestamp":1788797543602,"version":"build-2803163510"},"reference-count":253,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T00:00:00Z","timestamp":1788739200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T00:00:00Z","timestamp":1788739200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"DOI":"10.13039\/501100004829","name":"Science and Technology Department of Sichuan Province","doi-asserted-by":"publisher","award":["(26GJHZ0480)"],"award-info":[{"award-number":["(26GJHZ0480)"]}],"id":[{"id":"10.13039\/501100004829","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Mol Biomed"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    A20, encoded by tumor necrosis factor alpha-induced protein 3 (\n                    <jats:italic>TNFAIP3<\/jats:italic>\n                    ), is a ubiquitin-editing enzyme that acts as a central regulator of inflammatory signal termination, immune homeostasis and tissue protection. By controlling receptor-proximal ubiquitin signaling, A20 limits the amplitude and duration of inflammatory responses and thereby restrains the transition from acute host defense to chronic tissue-damaging inflammation. Genetic, biochemical and disease-model studies have linked altered A20 expression or function to a broad spectrum of human disorders, including monogenic autoinflammation, autoimmunity, barrier and fibrotic diseases, infection and cancer. However, the literature remains fragmented across organ systems and recurrent signaling pathways, obscuring the conserved biological functions of A20 and the contexts in which these functions become pathogenic. Here, we examine the mechanisms governing A20 activation, recruitment and ubiquitin-editing logic, with emphasis on the distinct contributions of the ovarian tumor (OTU) domain and zinc-finger (ZnF) modules. The major biological functions of A20 are then organized into recurrent output modules, including immune-cell homeostasis, signal termination, coordination of cell-death programmes, and oxidative-stress or immunometabolic adaptation. Disease associations are discussed according to dominant pathological outputs and vulnerable cellular compartments rather than by repetitive pathway listing. Finally, the therapeutic implications of A20 are assessed, including its potential as a biomarker and context-dependent therapeutic node, together with the translational challenges posed by cell-type specificity, disease-stage dependence and immune risk. A20 emerges as a context-dependent regulator of inflammation, tissue remodeling and tumour progression with relevance for biomarker development and precision therapeutic targeting.\n                  <\/jats:p>","DOI":"10.1186\/s43556-026-00557-7","type":"journal-article","created":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T04:20:26Z","timestamp":1788754826000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets"],"prefix":"10.1186","volume":"7","author":[{"given":"Junying","family":"Hu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xingchen","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenqiao","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bing","family":"Zhong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2866-2340","authenticated-orcid":false,"given":"Feng","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,7]]},"reference":[{"key":"557_CR1","doi-asserted-by":"publisher","unstructured":"Schulthei\u00df C, Paschold L, Mohebiany AN, Escher M, Kattimani YM, M\u00fcller M, et al. A20 haploinsufficiency disturbs immune homeostasis and drives the transformation of lymphocytes with permissive antigen receptors. Sci Adv. 2024;10(34):eadl3975. https:\/\/doi.org\/10.1126\/sciadv.adl3975.","DOI":"10.1126\/sciadv.adl3975"},{"issue":"1","key":"557_CR2","doi-asserted-by":"publisher","first-page":"6358","DOI":"10.1038\/s41467-022-33767-y","volume":"13","author":"W Wang","year":"2022","unstructured":"Wang W, Bale S, Wei J, Yalavarthi B, Bhattacharyya D, Yan JJ, et al. Fibroblast A20 governs fibrosis susceptibility and its repression by DREAM promotes fibrosis in multiple organs. Nat Commun. 2022;13(1):6358. https:\/\/doi.org\/10.1038\/s41467-022-33767-y.","journal-title":"Nat Commun"},{"issue":"1","key":"557_CR3","doi-asserted-by":"publisher","first-page":"154","DOI":"10.1038\/s41392-025-02194-y","volume":"10","author":"H Li","year":"2025","unstructured":"Li H, Wu Y, Xiang L, Zhao Q, Liu L, Zhu Z, et al. A20 attenuates oxidized self-DNA-mediated inflammation in acute kidney injury. Signal Transduct Target Ther. 2025;10(1):154. https:\/\/doi.org\/10.1038\/s41392-025-02194-y.","journal-title":"Signal Transduct Target Ther"},{"issue":"12","key":"557_CR4","doi-asserted-by":"publisher","DOI":"10.1002\/eji.202451245","volume":"54","author":"G Dabbah-Krancher","year":"2024","unstructured":"Dabbah-Krancher G, Ruchinskas A, Kallarakal MA, Lee KP, Bauman BM, Epstein B, et al. A20 intrinsically influences human effector T-cell survival and function by regulating both NF-\u03baB and JNK signaling. Eur J Immunol. 2024;54(12):e2451245. https:\/\/doi.org\/10.1002\/eji.202451245.","journal-title":"Eur J Immunol"},{"key":"557_CR5","doi-asserted-by":"publisher","unstructured":"K\u00f6hler P, Ribeiro A, Honarpisheh M, von Rauchhaupt E, Lorenz G, Li C, et al. Podocyte A20\/TNFAIP3 Controls glomerulonephritis severity via the regulation of inflammatory responses and effects on the cytoskeleton. Cells. 2025;14(5). https:\/\/doi.org\/10.3390\/cells14050381.","DOI":"10.3390\/cells14050381"},{"key":"557_CR6","doi-asserted-by":"publisher","first-page":"1373745","DOI":"10.3389\/fimmu.2024.1373745","volume":"15","author":"I Petta","year":"2024","unstructured":"Petta I, Thorp M, Ciers M, Blancke G, Boon L, Meese T, et al. Myeloid A20 is critical for alternative macrophage polarization and type-2 immune-mediated helminth resistance. Front Immunol. 2024;15:1373745. https:\/\/doi.org\/10.3389\/fimmu.2024.1373745.","journal-title":"Front Immunol"},{"issue":"3","key":"557_CR7","doi-asserted-by":"publisher","first-page":"76","DOI":"10.1007\/s10875-024-01681-1","volume":"44","author":"U Karri","year":"2024","unstructured":"Karri U, Harasimowicz M, Carpio Tumba M, Schwartz DM. The Complexity of Being A20: From Biological Functions to Genetic Associations. 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A20 mRNA therapeutics ameliorate systemic sclerosis by suppressing TRAF-6\/NF-KB signaling and DREAM expression and exerting antifibrotic effects. Front Immunol. 2025;16:1665998. https:\/\/doi.org\/10.3389\/fimmu.2025.1665998.","journal-title":"Front Immunol"},{"issue":"12","key":"557_CR11","doi-asserted-by":"publisher","first-page":"904","DOI":"10.1038\/s41419-024-07293-2","volume":"15","author":"M Qiu","year":"2024","unstructured":"Qiu M, Zhang W, Dai J, Sun W, Lai M, Tang S, et al. A20 negatively regulates necroptosis-induced microglia\/macrophages polarization and mediates cerebral ischemic tolerance via inhibiting the ubiquitination of RIP3. 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