| First Author | Tudor C | Year | 2009 |
| Journal | FEBS Lett | Volume | 583 |
| Issue | 12 | Pages | 1933-8 |
| PubMed ID | 19416727 | Mgi Jnum | J:150022 |
| Mgi Id | MGI:3849547 | Doi | 10.1016/j.febslet.2009.04.039 |
| Citation | Tudor C, et al. (2009) The p38 MAPK pathway inhibits tristetraprolin-directed decay of interleukin-10 and pro-inflammatory mediator mRNAs in murine macrophages. FEBS Lett 583(12):1933-8 |
| abstractText | p38 mitogen-activated protein kinase (MAPK) stabilises pro-inflammatory mediator mRNAs by inhibiting AU-rich element (ARE)-mediated decay. We show that in bone-marrow derived murine macrophages tristetraprolin (TTP) is necessary for the p38 MAPK-sensitive decay of several pro-inflammatory mRNAs, including cyclooxygenase-2 and the novel targets interleukin (IL)-6, and IL-1alpha. TTP(-/-) macrophages also strongly overexpress IL-10, an anti-inflammatory cytokine that constrains the production of the IL-6 despite its disregulation at the post-transcriptional level. TTP directly controls IL-10 mRNA stability, which is increased and insensitive to inhibition of p38 MAPK in TTP(-/-) macrophages. Furthermore, TTP enhances deadenylation of an IL-10 3'-untranslated region RNA in vitro. |
