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dc.contributor.authorHolloway, G
dc.contributor.authorCoulson, BS
dc.date.available2014-05-21T19:31:36Z
dc.date.issued2006-11-01
dc.identifierpii: JVI.00390-06
dc.identifier.citationHolloway, G. & Coulson, B. S. (2006). Rotavirus activates JNK and p38 signaling pathways in intestinal cells, leading to AP-1-driven transcriptional responses and enhanced virus replication. JOURNAL OF VIROLOGY, 80 (21), pp.10624-10633. https://doi.org/10.1128/JVI.00390-06.
dc.identifier.issn0022-538X
dc.identifier.urihttp://hdl.handle.net/11343/26411
dc.descriptionC1 - Journal Articles Refereed
dc.description.abstractRotavirus infection is known to regulate transcriptional changes in many cellular genes. The transcription factors NF-kappaB and AP-1 are activated by rotavirus infection, but the upstream processes leading to these events are largely unidentified. We therefore studied the activation state during rotavirus infection of c-Jun NH2-terminal kinase (JNK) and p38, which are kinases known to activate AP-1. As assessed by Western blotting using phospho-specific antibodies, infection with rhesus rotavirus (RRV) or exposure to UV-psoralen-inactivated RRV (I-RRV) resulted in the activation of JNK in HT-29, Caco-2, and MA104 cells. Activation of p38 during RRV infection was observed in Caco-2 and MA104 cells but not in HT-29 cells, whereas exposure to I-RRV did not lead to p38 activation in these cell lines. Rotavirus strains SA11, CRW-8, Wa, and UK also activated JNK and p38. Consistent with the activation of JNK, a corresponding increase in the phosphorylation of the AP-1 component c-Jun was shown. The interleukin-8 (IL-8) and c-jun promoters contain AP-1 binding sequences, and these genes have been shown previously to be transcriptionally up-regulated during rotavirus infection. Using specific inhibitors of JNK (SP600125) and p38 (SB203580) and real-time PCR, we showed that maximal RRV-induced IL-8 and c-jun transcription required JNK and p38 activity. This highlights the importance of JNK and p38 in RRV-induced, AP-1-driven gene expression. Significantly, inhibition of p38 or JNK in Caco-2 cells reduced RRV growth but not viral structural antigen expression, demonstrating the potential importance of JNK and p38 activation for optimal rotavirus replication.
dc.formatapplication/pdf
dc.languageEnglish
dc.publisherAMER SOC MICROBIOLOGY
dc.subjectMedical Virology ; Infectious Diseases
dc.titleRotavirus activates JNK and p38 signaling pathways in intestinal cells, leading to AP-1-driven transcriptional responses and enhanced virus replication
dc.typeJournal Article
dc.identifier.doi10.1128/JVI.00390-06
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliation.departmentMicrobiology And Immunology
melbourne.source.titleJournal of Virology
melbourne.source.volume80
melbourne.source.issue21
melbourne.source.pages10624-10633
melbourne.identifier.nhmrc350253
melbourne.identifier.nhmrc299862
melbourne.identifier.nhmrc350252
melbourne.publicationid50339
melbourne.elementsid276468
melbourne.openaccess.pmchttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1641755
melbourne.contributor.authorHolloway, Gavan
melbourne.contributor.authorCoulson, Barbara
dc.identifier.eissn1098-5514
melbourne.identifier.fundernameidNHMRC, 350253
melbourne.identifier.fundernameidNHMRC, 299862
melbourne.identifier.fundernameidNHMRC, 350252
melbourne.accessrightsAccess this item via the Open Access location


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