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Genetic variations in A20 DUB domain provide a genetic link to citrullination and neutrophil extracellular traps in systemic lupus erythematosus.

Lina Odqvist | Zala Jevnikar | Rebecca Riise | Lisa Öberg | Magdalena Rhedin | Dag Leonard | Linda Yrlid | Sonya Jackson | Johan Mattsson | Sambit Nanda | Philip Cohen | Axel Knebel | Simon Arthur | Kristofer Thörn | Elisabet Svenungsson | Andreas Jönsen | Iva Gunnarsson | Karolina Tandre | Andrei Alexsson | Alf Kastbom | Solbritt Rantapää-Dahlqvist | Maija-Leena Eloranta | Ann-Christine Syvänen | Anders Bengtsson | Patrik Johansson | Johanna K Sandling | Christopher Sjöwall | Lars Rönnblom | Barry Collins | Outi Vaarala
Annals of the rheumatic diseases | 2019

Genetic variations in TNFAIP3 (A20) de-ubiquitinase (DUB) domain increase the risk of systemic lupus erythematosus (SLE) and rheumatoid arthritis. A20 is a negative regulator of NF-κB but the role of its DUB domain and related genetic variants remain unclear. We aimed to study the functional effects of A20 DUB-domain alterations in immune cells and understand its link to SLE pathogenesis.

Pubmed ID: 31300459

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Associated grants

  • Agency: Medical Research Council, United Kingdom
    Id: MR/R021406/1
  • Agency: Medical Research Council, United Kingdom
    Id: MRC000985

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