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Splicing variant of WDFY4 augments MDA5 signalling and the risk of clinically amyopathic dermatomyositis.

Yuta KochiYoichiro KamataniYuya KondoAkari SuzukiEiryo KawakamiRyosuke HiwaYukihide MomozawaManabu FujimotoMasatoshi JinninYoshiya TanakaTakashi KandaRobert G CooperGabriela Arredondo Hector ChinoySimon RothwellJanine A LambJiří VencovskýHeřman MannKoichiro OhmuraKeiko MyouzenKazuyoshi IshigakiRan NakashimaYuji HosonoHiroto TsuboiHidenaga KawasumiYukiko IwasakiHiroshi KajiyamaTetsuya HoritaMariko Ogawa-MomoharaAkito TakamuraShinichiro TsunodaJun ShimizuKeishi FujioHirofumi AmanoAkio MimoriAtsushi KawakamiHisanori UmeharaTsutomu TakeuchiHajime SanoYoshinao MuroTatsuya AtsumiToshihide MimuraYasushi KawaguchiTsuneyo MimoriAtsushi TakahashiMichiaki KuboHitoshi KohsakaTakayuki SumidaKazuhiko Yamamoto
Published in: Annals of the rheumatic diseases (2018)
As CADM is characterised by the appearance of anti-MDA5 autoantibodies and severe lung inflammation, the WDFY4 variant may play a critical role in the pathogenesis of CADM.
Keyphrases
  • interstitial lung disease
  • breast cancer cells
  • systemic sclerosis
  • oxidative stress
  • systemic lupus erythematosus
  • cell cycle arrest
  • early onset
  • rheumatoid arthritis
  • disease activity
  • cell death
  • signaling pathway