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PP2A plays a key role in inflammation and cancer through tristetraprolin activation
  1. Ion Cristóbal1,
  2. Blanca Torrejón1,
  3. Juan Madoz-Gúrpide2,
  4. Federico Rojo2,
  5. Jesús García-Foncillas1
  1. 1Translational Oncology Division, Oncohealth Institute, IIS-Fundacion Jimenez Diaz, UAM, University Hospital ‘Fundacion Jimenez Diaz’, Madrid, Spain
  2. 2Pathology Department, University Hospital ‘Fundacion Jimenez Diaz’, Autonomous University of Madrid, Madrid, Spain
  1. Correspondence to Dr Ion Cristobal and Professor Jesús García-Foncillas, Translational Oncology Division, Oncohealth Institute, IIS-Fundacion Jimenez Diaz, UAM, University Hospital “Fundacion Jimenez Diaz”, Avda. Reyes Católicos-2, E-28040 Madrid, Spain; ion.cristobal{at}fjd.es, jgfoncillas{at}fjd.es

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We have read with great interest the recent work by Ross et al,1 which provides novel relevant findings about the therapeutic efficacy of using protein phosphatase 2A (PP2A)-activating drugs to target tristetraprolin (TTP) in rheumatoid arthritis (RA). In this elegant work, the authors showed that TTP is overexpressed and colocalises with activated mitogen-activated protein kinase (MAPK) p38 in RA synovial tissue. MAPK p38 phosphorylates and inhibits TTP at two serine residues, and Ross et al determined that these phosphorylation sites are critical for …

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