ArticleCellular and molecular life sciences : CMLS2022
A20 and ABIN-1 cooperate in balancing CBM complex-triggered NF-κB signaling in activated T cells.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- TNIP1 As A Potential Factor In Neuronal Survival, Growth and Differentiation in the Cerebellar Cortex.Cerebellum (London, England) · 2026Article
- PRMT7 restricts CD8+ T cells expansion via the NF-ΚB pathway.Nature communications · 2026Article
- A20 enhances the migration and metastasis of gastric cancer cells by promoting occludin degradation.Cell death discovery · 2026Article
- LUBAC modulates CBM complex functions downstream of TRAF6 in T cells.Nature communications · 2025Article
- Mesenchymal stromal cells conditioned by peripheral blood mononuclear cells exert enhanced immunomodulation capacities and alleviate a model of Myasthenia Gravis.Stem cell research & therapy · 2025Article
- Research Progress on the Role of Zinc Finger Protein in Colorectal Cancer.Cancer reports (Hoboken, N.J.) · 2025Review
- NF-κB regulated expression of A20 controls IKK dependent repression of RIPK1 induced cell death in activated T cells.Cell death and differentiation · 2025Article
- A20 intrinsically influences human effector T-cell survival and function by regulating both NF-κB and JNK signaling.European journal of immunology · 2024Article
- 4-1BB-encoding CAR causes cell death via sequestration of the ubiquitin-modifying enzyme A20.Cellular & molecular immunology · 2024Article
- ABIN1 is a negative regulator of effector functions in cytotoxic T cells.EMBO reports · 2024Article
- Genetic Mutations Associated With TNFAIP3 (A20) Haploinsufficiency and Their Impact on Inflammatory Diseases.International journal of molecular sciences · 2024Review
- Identification of gut microbes-related molecular subtypes and their biomarkers in colorectal cancer.Aging · 2024Article
- MALT1 substrate cleavage: what is it good for?Frontiers in immunology · 2024Review
- TCR Signals Controlling Adaptive Immunity against Toxoplasma and Cancer.Advances in experimental medicine and biology · 2024Article
- Repressive Control of Keratinocyte Cytoplasmic Inflammatory Signaling.International journal of molecular sciences · 2023Review
- Mistuned NF-κB signaling in lymphocytes: lessons from relevant inborn errors of immunity.Clinical and experimental immunology · 2023Article
- Proteolytic Activity of the Paracaspase MALT1 Is Involved in Epithelial Restitution and Mucosal Healing.International journal of molecular sciences · 2023Article
- Current research into A20 mediation of allergic respiratory diseases and its potential usefulness as a therapeutic target.Frontiers in immunology · 2023Review
- Elevated IgE from attenuated CARD11 signaling: lessons from atopic mice and humans.Current opinion in immunology · 2022Review
- CARMA3: A potential therapeutic target in non-cancer diseases.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
T cell activation initiates protective adaptive immunity, but counterbalancing mechanisms are critical to prevent overshooting responses and to maintain immune homeostasis. The CARD11-BCL10-MALT1 (CBM) complex bridges T cell receptor engagement to NF-κB signaling and MALT1 protease activation. Here, we show that ABIN-1 is modulating the suppressive function of A20 in T cells. Using quantitative mass spectrometry, we identified ABIN-1 as an interactor of the CBM signalosome in activated T cells. A20 and ABIN-1 counteract inducible activation of human primary CD4 and Jurkat T cells. While A20 overexpression is able to silence CBM complex-triggered NF-κB and MALT1 protease activation independent of ABIN-1, the negative regulatory function of ABIN-1 depends on A20. The suppressive function of A20 in T cells relies on ubiquitin binding through the C-terminal zinc finger (ZnF)4/7 motifs, but does not involve the deubiquitinating activity of the OTU domain. Our mechanistic studies reveal that the A20/ABIN-1 module is recruited to the CBM complex via A20 ZnF4/7 and that proteasomal degradation of A20 and ABIN-1 releases the CBM complex from the negative impact of both regulators. Ubiquitin binding to A20 ZnF4/7 promotes destructive K48-polyubiquitination to itself and to ABIN-1. Further, after prolonged T cell stimulation, ABIN-1 antagonizes MALT1-catalyzed cleavage of re-synthesized A20 and thereby diminishes sustained CBM complex signaling. Taken together, interdependent post-translational mechanisms are tightly controlling expression and activity of the A20/ABIN-1 silencing module and the cooperative action of both negative regulators is critical to balance CBM complex signaling and T cell activation.
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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.