| http://purl.uniprot.org/citations/20837746 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20837746 | http://www.w3.org/2000/01/rdf-schema#comment | "IFN-β and sIL-1Ra play crucial roles in the regulation of innate immunity and inflammation. IFN-β, which is widely used to improve the course of relapsing, remitting multiple sclerosis, induces the production of sIL-1Ra in human monocytes through mechanisms that remain largely unknown. In this study, we identified PI3Kδ and MEK2 as key elements that control sIL-1Ra production in isolated human monocytes activated by IFN-β. Blockade of MEK2, but not of MEK1, by inhibitors and siRNA prevented IFN-β-induced PI3Kδ recruitment to the membrane, Akt phosphorylation, and sIL-1Ra production, suggesting that MEK2 acted upstream of PI3Kδ. Furthermore, ERK1/2, the only identified substrates of MEK1/2 to date, are dispensable for sIL-1Ra production in response to IFN-β stimulation. Upon IFN-β activation, MEK2 and PI3Kδ are translocated to monocyte membranes. These data suggest that MEK1 and MEK2 display different, nonredundant functions in IFN-β signaling. That neither MEK1 nor ERK1/2 play a part in this mechanism is also an unexpected finding that gives rise to a better understanding of the MAPK signaling network. Together, these findings demonstrate that IFN-β triggers an atypical MEK2/PI3Kδ signaling cascade to regulate sIL-1Ra expression in monocytes. The premise that MEK1 and MEK2 play a part in the induction of the proinflammatory cytokine, IL-1β in human monocytes provides a rationale for an alternative, IFN-β-mediated pathway to induce/enhance sIL-1Ra production and thus, to dampen inflammation."xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.org/dc/terms/identifier | "doi:10.1189/jlb.0510312"xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/author | "Burger D."xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/author | "Gruaz L."xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/author | "Molnarfi N."xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/author | "Carpintero R."xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/author | "Brandt K.J."xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/name | "J Leukoc Biol"xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/pages | "1191-1200"xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/title | "A novel MEK2/PI3Kdelta pathway controls the expression of IL-1 receptor antagonist in IFN-beta-activated human monocytes."xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://purl.uniprot.org/core/volume | "88"xsd:string |
| http://purl.uniprot.org/citations/20837746 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/20837746 |
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