| http://purl.uniprot.org/citations/17609264 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17609264 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17609264 | http://www.w3.org/2000/01/rdf-schema#comment | "Epstein-Barr virus (EBV) infection of primary B cells causes B-cell activation and proliferation. Activation of B cells requires binding of antigen to the B-cell receptor and a survival signal from ligand-bound CD40, signals that are provided by the EBV LMP1 and LMP2A latency proteins. Recently, Toll-like receptor (TLR) signaling has been reported to provide a third B-cell activation stimulus. The interaction between the EBV and TLR pathways was therefore investigated. Both UV-inactivated and untreated EBV upregulated the expression of TLR7 and downregulated the expression of TLR9 in naive B cells. UV-inactivated virus transiently stimulated naive B-cell proliferation in the presence of the TLR7 ligand R837, while addition of the TLR7 antagonist IRS 661 impaired cell growth induced by untreated EBV. Interferon regulatory factor 5 (IRF-5) is a downstream mediator of TLR7 signaling. IRF-5 was induced following EBV infection, and IRF-5 was expressed in B-cell lines with type III latency. Expression of IRF-5 in this setting is surprising since IRF-5 has tumor suppressor and antiviral properties. B-cell proliferation assays provided evidence that EBV modulates TLR7 signaling responses. Examination of IRF-5 transcripts identified a novel splice variant, V12, that was induced by EBV infection, was constitutively nuclear, and acted as a dominant negative form in IRF-5 reporter assays. IRF-4 negatively regulates IRF-5 activation, and IRF-4 was also present in type III latently infected cells. EBV therefore initially uses TLR7 signaling to enhance B-cell proliferation and subsequently modifies the pathway to regulate IRF-5 activity."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.org/dc/terms/identifier | "doi:10.1128/JVI.01122-07"xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.org/dc/terms/identifier | "doi:10.1128/jvi.01122-07"xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/author | "Hayward S.D."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/author | "Hayward S.D."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/author | "Lee J.M."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/author | "Lee J.M."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/author | "Martin H.J."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/author | "Martin H.J."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/author | "Walls D."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/author | "Walls D."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/name | "J. Virol."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/name | "J Virol"xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/pages | "9748-9758"xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/pages | "9748-9758"xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/title | "Manipulation of the toll-like receptor 7 signaling pathway by Epstein-Barr virus."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/title | "Manipulation of the toll-like receptor 7 signaling pathway by Epstein-Barr virus."xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/volume | "81"xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://purl.uniprot.org/core/volume | "81"xsd:string |
| http://purl.uniprot.org/citations/17609264 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17609264 |
| http://purl.uniprot.org/citations/17609264 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17609264 |