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RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury
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The deubiquitinase activity of A20 is dispensable for NF-κB signaling
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Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis
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A20 inhibits LUBAC-mediated NF-κB activation by binding linear polyubiquitin chains via its zinc finger 7
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B cells lacking the tumor suppressor TNFAIP3/A20 display impaired differentiation and hyperactivation and cause inflammation and autoimmunity in aged mice
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A20 (TNFAIP3) deficiency in myeloid cells triggers erosive polyarthritis resembling rheumatoid arthritis
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Expression of A20 by dendritic cells preserves immune homeostasis and prevents colitis and spondyloarthritis
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Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis
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De-ubiquitination and ubiquitin ligase domains of A20 downregulate NF-κB signalling
IE Wertz et al.
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TNF-mediated inflammatory skin disease in mice with epidermis-specific deletion of IKK2
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Failure to regulate TNF-induced NF-κB and cell death responses in A20-deficient mice
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