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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.
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