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000128288 0247_ $$2doi$$a10.1371/journal.pgen.1004368
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000128288 041__ $$aeng
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000128288 1001_ $$0P:(DE-He78)1bd20c9facf01a9dd3eae38ef6a7e137$$aSchott, Johanna$$b0$$eFirst author$$udkfz
000128288 245__ $$aTranslational regulation of specific mRNAs controls feedback inhibition and survival during macrophage activation.
000128288 260__ $$aSan Francisco, Calif.$$bPublic Library of Science$$c2014
000128288 3367_ $$2DRIVER$$aarticle
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000128288 520__ $$aFor a rapid induction and efficient resolution of the inflammatory response, gene expression in cells of the immune system is tightly regulated at the transcriptional and post-transcriptional level. The control of mRNA translation has emerged as an important determinant of protein levels, yet its role in macrophage activation is not well understood. We systematically analyzed the contribution of translational regulation to the early phase of the macrophage response by polysome fractionation from mouse macrophages stimulated with lipopolysaccharide (LPS). Individual mRNAs whose translation is specifically regulated during macrophage activation were identified by microarray analysis. Stimulation with LPS for 1 h caused translational activation of many feedback inhibitors of the inflammatory response including NF-κB inhibitors (Nfkbid, Nfkbiz, Nr4a1, Ier3), a p38 MAPK antagonist (Dusp1) and post-transcriptional suppressors of cytokine expression (Zfp36 and Zc3h12a). Our analysis showed that their translation is repressed in resting and de-repressed in activated macrophages. Quantification of mRNA levels at a high temporal resolution by RNASeq allowed us to define groups with different expression patterns. Thereby, we were able to distinguish mRNAs whose translation is actively regulated from mRNAs whose polysomal shifts are due to changes in mRNA levels. Active up-regulation of translation was associated with a higher content in AU-rich elements (AREs). For one example, Ier3 mRNA, we show that repression in resting cells as well as de-repression after stimulation depends on the ARE. Bone-marrow derived macrophages from Ier3 knockout mice showed reduced survival upon activation, indicating that IER3 induction protects macrophages from LPS-induced cell death. Taken together, our analysis reveals that translational control during macrophage activation is important for cellular survival as well as the expression of anti-inflammatory feedback inhibitors that promote the resolution of inflammation.
000128288 536__ $$0G:(DE-HGF)POF3-311$$a311 - Signalling pathways, cell and tumor biology (POF3-311)$$cPOF3-311$$fPOF III$$x0
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000128288 650_7 $$2NLM Chemicals$$aAdaptor Proteins, Signal Transducing
000128288 650_7 $$2NLM Chemicals$$aCytokines
000128288 650_7 $$2NLM Chemicals$$aIEX-1 protein, mouse
000128288 650_7 $$2NLM Chemicals$$aImmediate-Early Proteins
000128288 650_7 $$2NLM Chemicals$$aLipopolysaccharides
000128288 650_7 $$2NLM Chemicals$$aNF-kappa B
000128288 650_7 $$2NLM Chemicals$$aNfkbiz protein, mouse
000128288 650_7 $$2NLM Chemicals$$aNr4a1 protein, mouse
000128288 650_7 $$2NLM Chemicals$$aNuclear Proteins
000128288 650_7 $$2NLM Chemicals$$aNuclear Receptor Subfamily 4, Group A, Member 1
000128288 650_7 $$2NLM Chemicals$$aRNA, Messenger
000128288 650_7 $$2NLM Chemicals$$aTristetraprolin
000128288 650_7 $$2NLM Chemicals$$aZfp36 protein, mouse
000128288 650_7 $$0EC 2.7.11.24$$2NLM Chemicals$$ap38 Mitogen-Activated Protein Kinases
000128288 650_7 $$0EC 3.1.-$$2NLM Chemicals$$aRibonucleases
000128288 650_7 $$0EC 3.1.-$$2NLM Chemicals$$aZc3h12a protein, mouse
000128288 650_7 $$0EC 3.1.3.48$$2NLM Chemicals$$aDual Specificity Phosphatase 1
000128288 650_7 $$0EC 3.1.3.48$$2NLM Chemicals$$aDusp1 protein, mouse
000128288 7001_ $$0P:(DE-He78)d1bdeec6c1345e82a575125e894c5283$$aReitter, Sonja$$b1$$udkfz
000128288 7001_ $$0P:(DE-HGF)0$$aPhilipp, Janine$$b2
000128288 7001_ $$0P:(DE-HGF)0$$aHaneke, Katharina$$b3
000128288 7001_ $$aSchäfer, Heiner$$b4
000128288 7001_ $$0P:(DE-HGF)0$$aStoecklin, Georg$$b5$$eLast author
000128288 773__ $$0PERI:(DE-600)2186725-2$$a10.1371/journal.pgen.1004368$$gVol. 10, no. 6, p. e1004368 -$$n6$$pe1004368 -$$tPLoS Genetics$$v10$$x1553-7404$$y2014
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