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• W4301183285 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." @default.
• W4301183285 created "2022-10-04" @default.
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• W4301183285 date "2022-10-04" @default.
• W4301183285 modified "2023-10-16" @default.
• W4301183285 title "<scp>A20</scp> controls <scp>RANK</scp> ‐dependent osteoclast formation and bone physiology" @default.
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• W4301183285 doi "https://doi.org/10.15252/embr.202255233" @default.
• W4301183285 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36194667" @default.
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