ArticleCells2020
A20 Promotes Ripoptosome Formation and TNF-Induced Apoptosis via cIAPs Regulation and NIK Stabilization in Keratinocytes.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Genetic Mutations Associated With TNFAIP3 (A20) Haploinsufficiency and Their Impact on Inflammatory Diseases.International journal of molecular sciences · 2024Review
- A20 in Kidney Transplantation and Autoimmunity.International journal of molecular sciences · 2024Review
- The Role of the NF-kB Pathway in Intracranial Aneurysms.Brain sciences · 2023Review
- Repressive Control of Keratinocyte Cytoplasmic Inflammatory Signaling.International journal of molecular sciences · 2023Review
- A biochemical necroptosis model explains cell-type-specific responses to cell death cues.Biophysical journal · 2023Article
- The role of pyroptosis in inflammatory diseases.Frontiers in cell and developmental biology · 2023Review
- RIPK1 in the inflammatory response and sepsis: Recent advances, drug discovery and beyond.Frontiers in immunology · 2023Review
- Advances in the Study of the Ubiquitin-Editing Enzyme A20.Frontiers in pharmacology · 2022Review
- RIPK1 and TRADD Regulate TNF-Induced Signaling and Ripoptosome Formation.International journal of molecular sciences · 2021Article
- Deubiquitinases: Modulators of Different Types of Regulated Cell Death.International journal of molecular sciences · 2021Review
- Very Early Involvement of Innate Immunity in Peripheral Nerve Degeneration in SOD1-G93A Mice.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ubiquitin-editing protein A20 (TNFAIP3) is a known key player in the regulation of immune responses in many organs. Genome-wide associated studies (GWASs) have linked A20 with a number of inflammatory and autoimmune disorders, including psoriasis. Here, we identified a previously unrecognized role of A20 as a pro-apoptotic factor in TNF-induced cell death in keratinocytes. This function of A20 is mediated via the NF-κB-dependent alteration of cIAP1/2 expression. The changes in cIAP1/2 protein levels promote NIK stabilization and subsequent activation of noncanonical NF-κB signaling. Upregulation of TRAF1 expression triggered by the noncanonical NF-κB signaling further enhances the NIK stabilization in an autocrine manner. Finally, stabilized NIK promotes the formation of the ripoptosome and the execution of cell death. Thus, our data demonstrate that A20 controls the execution of TNF-induced cell death on multiple levels in keratinocytes. This signaling mechanism might have important implications for the development of new therapeutic strategies for the treatment of A20-associated skin diseases.
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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.