Non-catalytic ubiquitin binding by A20 prevents psoriatic arthritis-like disease and inflammation
暂无分享,去创建一个
P. Turnbaugh | Francis S. Kim | P. Achacoso | Jessie A. Turnbaugh | A. Ma | B. Malynn | M. Whang | Rommel Advincula | Mary C. Nakamura | Xiaofei Sun | M. Pendse | Bahram Razani | Priscilia Tanbun
[1] A. Ma,et al. A20: A multifunctional tool for regulating immunity and preventing disease. , 2019, Cellular immunology.
[2] G. Kollias,et al. A20 prevents inflammasome-dependent arthritis by inhibiting macrophage necroptosis through its ZnF7 ubiquitin-binding domain , 2019, Nature Cell Biology.
[3] M. McDermott,et al. Faculty Opinions recommendation of A20 haploinsufficiency (HA20): clinical phenotypes and disease course of patients with a newly recognised NF-kB-mediated autoinflammatory disease. , 2019, Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature.
[4] P. Miossec,et al. IL-17 in Rheumatoid Arthritis and Precision Medicine: From Synovitis Expression to Circulating Bioactive Levels , 2019, Front. Med..
[5] A. Blauvelt,et al. The Immunologic Role of IL-17 in Psoriasis and Psoriatic Arthritis Pathogenesis , 2018, Clinical Reviews in Allergy & Immunology.
[6] I. Touitou,et al. Autosomic dominant familial Behçet disease and haploinsufficiency A20: A review of the literature. , 2018, Autoimmunity reviews.
[7] N. Hacohen,et al. Defining inflammatory cell states in rheumatoid arthritis joint synovial tissues by integrating single-cell transcriptomics and mass cytometry , 2018, bioRxiv.
[8] D. Veale,et al. The pathogenesis of psoriatic arthritis , 2018, The Lancet.
[9] I. Touitou,et al. ‘A20 haploinsufficiency (HA20): clinical phenotypes and disease course of patients with a newly recognised NF-kB-mediated autoinflammatory disease’ , 2018, Annals of the rheumatic diseases.
[10] D. Kastner,et al. A20 haploinsufficiency (HA20): clinical phenotypes and disease course of patients with a newly recognised NF-kB-mediated autoinflammatory disease , 2018, Annals of the rheumatic diseases.
[11] O. Ohara,et al. Haploinsufficiency of A20 causes autoinflammatory and autoimmune disorders. , 2017, The Journal of allergy and clinical immunology.
[12] A. Ma,et al. Hypomorphic A20 expression confers susceptibility to psoriasis , 2017, PloS one.
[13] J. Orange,et al. Recruitment of A20 by the C-terminal domain of NEMO suppresses NF-κB activation and autoinflammatory disease , 2016, Proceedings of the National Academy of Sciences.
[14] Jinfeng Liu,et al. Phosphorylation and linear ubiquitin direct A20 inhibition of inflammation , 2015, Nature.
[15] J. Mullikin,et al. Loss-of-function mutations in TNFAIP3 leading to A20 haploinsufficiency cause an early onset autoinflammatory syndrome , 2015, Nature Genetics.
[16] K. Rittinger,et al. LUBAC-Recruited CYLD and A20 Regulate Gene Activation and Cell Death by Exerting Opposing Effects on Linear Ubiquitin in Signaling Complexes , 2015, Cell reports.
[17] H. Hammad,et al. Farm dust and endotoxin protect against allergy through A20 induction in lung epithelial cells , 2015, Science.
[18] A. Burlingame,et al. The ubiquitin-modifying enzyme A20 restricts the ubiquitination of RIPK3 and protects cells from necroptosis , 2015, Nature Immunology.
[19] A. Burlingame,et al. A20 restricts ubiquitination of pro-interleukin-1β protein complexes and suppresses NLRP3 inflammasome activity. , 2015, Immunity.
[20] Arnab De,et al. The deubiquitinase activity of A20 is dispensable for NF‐κB signaling , 2014, EMBO reports.
[21] G. van Loo,et al. Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis , 2014, Nature.
[22] C. Huttenhower,et al. Expansion of intestinal Prevotella copri correlates with enhanced susceptibility to arthritis , 2013, eLife.
[23] Patrick G. A. Pedrioli,et al. Activation of the canonical IKK complex by K63/M1-linked hybrid ubiquitin chains , 2013, Proceedings of the National Academy of Sciences.
[24] George Kollias,et al. Proof of concept: enthesitis and new bone formation in spondyloarthritis are driven by mechanical strain and stromal cells , 2013, Annals of the rheumatic diseases.
[25] Hao Wu,et al. Dimerization and ubiquitin mediated recruitment of A20, a complex deubiquitinating enzyme. , 2013, Immunity.
[26] I. Dikic,et al. A20 inhibits LUBAC‐mediated NF‐κB activation by binding linear polyubiquitin chains via its zinc finger 7 , 2012, The EMBO journal.
[27] H. Nishimasu,et al. Specific recognition of linear polyubiquitin by A20 zinc finger 7 is involved in NF‐κB regulation , 2012, The EMBO journal.
[28] Jin He,et al. Direct, noncatalytic mechanism of IKK inhibition by A20. , 2011, Molecular cell.
[29] E. Huang,et al. Dendritic cell expression of A20 preserves immune homeostasis and prevents colitis and spondyloarthritis , 2011, Nature Immunology.
[30] M. Kool,et al. A20 (TNFAIP3) deficiency in myeloid cells triggers erosive polyarthritis resembling rheumatoid arthritis , 2011, Nature Genetics.
[31] H. Hammad,et al. The ubiquitin-editing protein A20 prevents dendritic cell activation, recognition of apoptotic cells, and systemic autoimmunity. , 2011, Immunity.
[32] V. Dixit,et al. Ubiquitin binding to A20 ZnF4 is required for modulation of NF-κB signaling. , 2010, Molecular cell.
[33] C. Liu,et al. The ubiquitin modifying enzyme A20 restricts B cell survival and prevents autoimmunity. , 2010, Immunity.
[34] Christophe Benoist,et al. Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells. , 2010, Immunity.
[35] Noula Shembade,et al. Inhibition of NF-κB Signaling by A20 Through Disruption of Ubiquitin Enzyme Complexes , 2010, Science.
[36] Dan R. Littman,et al. Induction of Intestinal Th17 Cells by Segmented Filamentous Bacteria , 2009, Cell.
[37] Yusuke Sato,et al. Structural basis for specific recognition of Lys 63‐linked polyubiquitin chains by tandem UIMs of RAP80 , 2009, The EMBO journal.
[38] Joshua J. Sims,et al. Linkage-specific avidity defines the lysine 63-linked polyubiquitin-binding preference of rap80. , 2009, Molecular cell.
[39] D. Baltimore,et al. The stability of mRNA influences the temporal order of the induction of genes encoding inflammatory molecules , 2009, Nature Immunology.
[40] Bettina L. Lee,et al. Homeostatic MyD88-dependent signals cause lethal inflamMation in the absence of A20 , 2008, The Journal of experimental medicine.
[41] George Kollias,et al. Mesenchymal cell targeting by TNF as a common pathogenic principle in chronic inflammatory joint and intestinal diseases , 2008, The Journal of experimental medicine.
[42] Y. Lo,et al. Molecular basis for the unique deubiquitinating activity of the NF-kappaB inhibitor A20. , 2008, Journal of molecular biology.
[43] S. Gabriel,et al. Two independent alleles at 6q23 associated with risk of rheumatoid arthritis , 2007, Nature Genetics.
[44] Georg Schett,et al. Cytokines in the pathogenesis of rheumatoid arthritis , 2007, Nature Reviews Immunology.
[45] Matthew T Wheeler,et al. The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses , 2004, Nature Immunology.
[46] Somasekar Seshagiri,et al. De-ubiquitination and ubiquitin ligase domains of A20 downregulate NF-κB signalling , 2004, Nature.
[47] D. Wallach. Faculty Opinions recommendation of De-ubiquitination and ubiquitin ligase domains of A20 downregulate NF-kappaB signalling. , 2004 .
[48] A. Hoffmann,et al. The I (cid:1) B –NF-(cid:1) B Signaling Module: Temporal Control and Selective Gene Activation , 2022 .
[49] A. Ma,et al. Failure to regulate TNF-induced NF-kappaB and cell death responses in A20-deficient mice. , 2000, Science.
[50] J. Woody,et al. Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor α (cA2) versus placebo in rheumatoid arthritis , 1994, The Lancet.
[51] D. Gladman,et al. Psoriatic Arthritis. , 2017, The New England journal of medicine.
[52] L. Catrysse,et al. A20 in inflammation and autoimmunity. , 2014, Trends in immunology.
[53] A. R.,et al. Review of literature , 1969, American Potato Journal.
[54] A. Hoffmann,et al. The IkappaB-NF-kappaB signaling module: temporal control and selective gene activation. , 2002, Science.
[55] W. Eyler,et al. PSORIATIC ARTHRITIS. , 1965, Henry Ford Hospital medical bulletin.