Amplification of JNK Signaling Is Necessary To Complete the Murine Gammaherpesvirus 68 Lytic Replication Cycle
| العنوان: | Amplification of JNK Signaling Is Necessary To Complete the Murine Gammaherpesvirus 68 Lytic Replication Cycle |
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| المؤلفون: | Clinton R. Paden, J. Craig Forrest, James A. Stahl, Samuel H. Speck, Veronica MacLeod, Ricky D. Edmondson, Shweta S. Chavan |
| المصدر: | Journal of Virology. 86:13253-13262 |
| بيانات النشر: | American Society for Microbiology, 2012. |
| سنة النشر: | 2012 |
| مصطلحات موضوعية: | MAP Kinase Kinase 4, viruses, Molecular Sequence Data, Immunology, Biology, Virus Replication, Microbiology, Mice, Viral Proteins, Gammaherpesvirinae, Tandem Mass Spectrometry, Transcription (biology), Viral entry, Virology, Gene expression, Animals, Humans, Amino Acid Sequence, Kinase, Virus-Cell Interactions, Cell biology, Mice, Inbred C57BL, Viral replication, Lytic cycle, Insect Science, Phosphorylation, Signal transduction, Signal Transduction |
| الوصف: | Several studies have previously defined host-derived signaling events capable of driving lytic gammaherpesvirus replication or enhancing immediate-early viral gene expression. Yet signaling pathways that regulate later stages of the productive gammaherpesvirus replication cycle are still poorly defined. In this study, we utilized a mass spectrometric approach to identify c-Jun as an abundant cellular phosphoprotein present in late stages of lytic murine gammaherpesvirus 68 (MHV68) infection. Kinetically, c-Jun phosphorylation was enhanced as infection progressed, and this correlated with enhanced phosphorylation of the c-Jun amino-terminal kinases JNK1 and JNK2 and activation of AP-1 transcription. These events were dependent on progression beyond viral immediate-early gene expression, but not dependent on viral DNA replication. Both pharmacologic and dominant-negative blockade of JNK1/2 activity inhibited viral replication, and this correlated with inhibition of viral DNA synthesis and reduced viral gene expression. These data suggest a model in which MHV68 by necessity amplifies and usurps JNK/c-Jun signaling as infection progresses in order to facilitate late stages of the MHV68 lytic infection cycle. |
| تدمد: | 1098-5514 0022-538X |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::231200282c4a96965297c961333caeea https://doi.org/10.1128/jvi.01432-12 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....231200282c4a96965297c961333caeea |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10985514 0022538X |
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