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miami |
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|a 2045-2322
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|a urn:nbn:de:hbz:6-64269522380
|2 urn
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|a 10.1038/srep27275
|2 doi
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|a eng
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|a 610 Medizin und Gesundheit
|2 23
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|a Dudek, Sabine Eva
|0 http://d-nb.info/gnd/142709794
|4 aut
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|a Universitäts- und Landesbibliothek Münster
|0 http://d-nb.info/gnd/5091030-9
|4 own
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|a Influenza A viruses suppress cyclooxygenase-2 expression by affecting its mRNA stability
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|a [Electronic ed.]
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|c 2016-06-06
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|b Universitäts- und Landesbibliothek Münster
|c 2016-09-22
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|a 1-13
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|a Finanziert durch den Open-Access-Publikationsfonds 2015/2016 der Westfälischen Wilhelms-Universität Münster (WWU Münster).
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|a free access
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|a Scientific Reports 6 (2016) 27275, 1-13
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|a Infection with influenza A viruses (IAV) provokes activation of cellular defence mechanisms contributing to the innate immune and inflammatory response. In this process the cyclooxygenase-2 (COX-2) plays an important role in the induction of prostaglandin-dependent inflammation. While it has been reported that COX-2 is induced upon IAV infection, in the present study we observed a down-regulation at later stages of infection suggesting a tight regulation of COX-2 by IAV. Our data indicate the pattern-recognition receptor RIG-I as mediator of the initial IAV-induced COX-2 synthesis. Nonetheless, during on-going IAV replication substantial suppression of COX-2 mRNA and protein synthesis could be detected, accompanied by a decrease in mRNA half-life. Interestingly, COX-2 mRNA stability was not only imbalanced by IAV replication but also by stimulation of cells with viral RNA. Our results reveal tristetraprolin (TTP), which is known to bind COX-2 mRNA and promote its rapid degradation, as regulator of COX-2 expression in IAV infection. During IAV replication and viral RNA accumulation TTP mRNA synthesis was induced, resulting in reduced COX-2 levels. Accordingly, the down-regulation of TTP resulted in increased COX-2 protein expression after IAV infection. These findings indicate a novel IAV-regulated cellular mechanism, contributing to the repression of host defence and therefore facilitating viral replication.
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|a specialized
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|a CC BY 4.0
|u http://creativecommons.org/licenses/by/4.0/
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|2 DRIVER Types
|a Artikel
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|2 DCMI Types
|a Text
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|a Nitzsche, Katja
|0 http://d-nb.info/gnd/1064552420
|4 aut
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|a Ludwig, Stephan
|u FB 13: Biologie
|0 http://d-nb.info/gnd/1227972156
|0 https://orcid.org/0000-0003-4490-3052
|0 http://viaf.org/viaf/2087161453856964330002
|4 aut
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|a Ehrhardt, Christina
|0 http://d-nb.info/gnd/124517145
|4 aut
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|3 Zum Volltext
|q text/html
|u https://nbn-resolving.de/urn:nbn:de:hbz:6-64269522380
|u urn:nbn:de:hbz:6-64269522380
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|3 Zum Volltext
|q application/pdf
|u https://repositorium.uni-muenster.de/document/miami/0eb2a20d-cdf0-43a5-b073-1b04b51757f8/srep27275.pdf
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