The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses

By D. Boone, Emre E. Turer, Eric G. Lee, Regina-Celeste Ahmad, M. Wheeler, C. Tsui, P. Hurley, Marcia Chien, Sophia Chai, O. Hitotsumatsu and 3 more. Nature Immunology, 2004

1,168 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/b2d99efe55da5f9d9a5e796ec8747cc83b4a2953

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In Cancer Research

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In Immunology

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Citations in the corpus

• Mechanism and function of deubiquitinating enzymes. (2004, background): “Affinity purified A20 can disassemble both Ly48- and Lys63-linked ubiquitin chains [16,17,95].”
• Ubiquitin signalling in the NF-κB pathway (2005, background): “Another DUB that acts in this pathway is A20, an NF-κB-induced protein that inhibits NF-κB in a negative-feedback loo”
• Regulation of NF-κB by TNF Family Cytokines (2014, background): “Nevertheless, in vivo, it appears that A20 is not, primarily a regulator of TNF responses, but rather of TLR and IL-1R signaling, as the inflammatory phenotype of the A20 deficient mice is rescued by deletion of MyD88 but not TNFR1 or TNF [132, 133].”
• Negative regulation of Toll-like receptor-mediated immune responses (2005, background): “Macrophages from A20-deficient mice produced elevated levels of pro-inflammatory cytokines following stimulation with the TLR2 ligands peptidoglycan and lipoteichoic acid, the TLR3 ligand polyI:C and the TLR9 ligand CpG DN”
• Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “The mechanism of induction of IFN follows a different profile from dsRNA-induced activation of TLR3, in that ssRNA-activated TLR7 recruits a distinct adaptor called myeloid differentiation factor 88 (MyD88) that, in turn, recruits a complex containing the kinases interleukin-1 receptor-associated ki”
• Breaking the chains: structure and function of the deubiquitinases (2009, background): “Deficiency of A20 in mice causes persistent activation of NF-κB by Toll-like and TNF receptor”
• Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “Thus, molecular signaling mechanisms within the TRIF-dependent pathway illustrate how selective binding of different molecules, i.e., either TRAF3 or TRAF6, results in recruitment and downstream activation of TBK1-IRF versus TAK1-IKK-NF- B, respectively (Fig.”
• Pattern recognition receptors and inflammation. (2010, background): “A20 negatively regulates NF-kB activation downstream of TLR2 and NOD1/NOD2 (Boone et al., 2004; Hitotsumatsu et al., 2008).”