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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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