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10.1016/j.febslet.2009.04.039

http://scihub22266oqcxt.onion/10.1016/j.febslet.2009.04.039
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suck abstract from ncbi


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pmid19416727
      FEBS+Lett 2009 ; 583 (12 ): 1933-8
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  • The p38 MAPK pathway inhibits tristetraprolin-directed decay of interleukin-10 and pro-inflammatory mediator mRNAs in murine macrophages #MMPMID19416727
  • Tudor C ; Marchese FP ; Hitti E ; Aubareda A ; Rawlinson L ; Gaestel M ; Blackshear PJ ; Clark AR ; Saklatvala J ; Dean JL
  • FEBS Lett 2009[Jun]; 583 (12 ): 1933-8 PMID19416727 show ga
  • 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.
  • |Animals [MESH]
  • |Base Sequence [MESH]
  • |In Vitro Techniques [MESH]
  • |Inflammation Mediators/*metabolism [MESH]
  • |Interleukin-10/antagonists & inhibitors/*genetics [MESH]
  • |Interleukin-12 Subunit p40/biosynthesis [MESH]
  • |Interleukin-6/biosynthesis [MESH]
  • |MAP Kinase Signaling System [MESH]
  • |Macrophages/*metabolism [MESH]
  • |Mice [MESH]
  • |Mice, Inbred C57BL [MESH]
  • |Mice, Knockout [MESH]
  • |RNA Stability [MESH]
  • |RNA, Messenger/*genetics/*metabolism [MESH]
  • |Tristetraprolin/deficiency/genetics/*metabolism [MESH]


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