ArticleEMBO reports2022
A20 controls RANK-dependent osteoclast formation and bone physiology.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Iron, Copper, and Zinc Dyshomeostasis in Cardiovascular and Cerebrovascular Diseases: Redox Mechanisms, Evidence Levels, and Translational Prospects.International journal of molecular sciences · 2026Review
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- USP8-mediated mitochondrial regulation in osteoclasts is essential for skeletal development.Cellular and molecular life sciences : CMLS · 2026Article
- Unveiling the Therapeutic Targets and Active Components of Xianlinggubao Capsule in Osteoarthritis and Osteoporosis through Network Pharmacology and Bioinformatic Analysis.Current pharmaceutical design · 2026Article
- Integrative Transcriptomic and Machine-Learning Analysis Reveals Immune-Inflammatory and Stress-Response Alterations in MRONJ.International journal of molecular sciences · 2025Article
- Exploration of potential novel drug targets for rheumatoid arthritis by plasma proteome screening.PLoS computational biology · 2025Article
- The research potential of A20 in psoriatic arthritis.Frontiers in immunology · 2025Review
- Serum A20 level is associated with bone mineral density in male patients with type 2 diabetes mellitus.Frontiers in endocrinology · 2025Article
- TNF receptor-associated factors: promising targets of natural products for the treatment of osteoporosis.Frontiers in physiology · 2025Review
- OTUD1 inhibits osteoclast differentiation and osteoclastic bone loss through deubiquitinating and stabilizing PRDX1.Theranostics · 2025Article
- Osteogenesis imperfecta type 10 and the cellular scaffolds underlying common immunological diseases.Genes and immunity · 2024Review
- Identification of Long Non-Coding RNA as Potential Biomarkers for the Diagnosis of Postmenopausal Osteoporosis.International journal of endocrinology · 2024Article
- Association between polymorphisms of anti-inflammatory gene alleles and periodontitis risk in a Chinese Han population.Clinical oral investigations · 2023Article
- Roles of RIPK1 as a stress sentinel coordinating cell survival and immunogenic cell death.Nature reviews. Molecular cell biology · 2023Review
- Human osteoarthritic articular cartilage stem cells suppress osteoclasts and improve subchondral bone remodeling in experimental knee osteoarthritis partially by releasing TNFAIP3.Stem cell research & therapy · 2023Article
- RNA demethylase ALKBH5 suppresses tumorigenesis via inhibiting proliferation and invasion and promoting CD8Translational oncology · 2023Article
- Current research into A20 mediation of allergic respiratory diseases and its potential usefulness as a therapeutic target.Frontiers in immunology · 2023Review
- The Role of Sympathetic Nerves in Osteoporosis: A Narrative Review.Biomedicines · 2022Review
- A20 controls RANK-dependent osteoclast formation and bone physiology.EMBO reports · 2022Article
Corrections and comments
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Authors and funding
23 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anti-inflammatory protein A20 serves as a critical brake on NF-κB signaling and NF-κB-dependent inflammation. In humans, polymorphisms in or near the TNFAIP3/A20 gene have been associated with several inflammatory disorders, including rheumatoid arthritis (RA), and experimental studies in mice have demonstrated that myeloid-specific A20 deficiency causes the development of a severe polyarthritis resembling human RA. Myeloid A20 deficiency also promotes osteoclastogenesis in mice, suggesting a role for A20 in the regulation of osteoclast differentiation and bone formation. We show here that osteoclast-specific A20 knockout mice develop severe osteoporosis, but not inflammatory arthritis. In vitro, osteoclast precursor cells from A20 deficient mice are hyper-responsive to RANKL-induced osteoclastogenesis. Mechanistically, we show that A20 is recruited to the RANK receptor complex within minutes of ligand binding, where it restrains NF-κB activation independently of its deubiquitinating activity but through its zinc finger (ZnF) 4 and 7 ubiquitin-binding functions. Together, these data demonstrate that A20 acts as a regulator of RANK-induced NF-κB signaling to control osteoclast differentiation, assuring proper bone development and turnover.
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Registered trials
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.