| http://purl.uniprot.org/citations/26044139 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/26044139 | http://www.w3.org/2000/01/rdf-schema#comment | "Viruses are known to induce pathological cellular states that render infected cells susceptible or resistant to immune recognition. Here, we characterize an MHC-I-independent natural killer (NK) cell recognition mechanism that involves modulation of inhibitory NKR-P1B:Clr-b receptor-ligand interactions in response to mouse cytomegalovirus (MCMV) infection. We demonstrate that mouse Clr-b expression on healthy cells is rapidly lost at the cell surface and transcript levels in a time- and dose-dependent manner upon MCMV infection. In addition, cross-species infections using rat cytomegalovirus (RCMV) infection of mouse fibroblasts and MCMV infection of rat fibroblasts suggest that this response is conserved during host-pathogen interactions. Active viral infection appears to be necessary for Clr-b loss, as cellular stimulation using UV-inactivated whole virus or agonists of many innate pattern recognition receptors failed to elicit efficient Clr-b downregulation. Notably, Clr-b loss could be partially blocked by titrated cycloheximide treatment, suggesting that early viral or nascent host proteins are required for Clr-b downregulation. Interestingly, reporter cell assays suggest that MCMV may encode a novel Clr-b-independent immunoevasin that functionally engages the NKR-P1B receptor. Together, these data suggest that Clr-b modulation is a conserved innate host cell response to virus infection that is subverted by multiple CMV immune evasion strategies."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.org/dc/terms/identifier | "doi:10.1159/000382032"xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/author | "Chen P."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/author | "Ma J."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/author | "Voigt S."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/author | "Allan D.S."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/author | "Carlyle J.R."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/author | "Hundrieser J."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/author | "Mesci A."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/author | "Aguilar O.A."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/author | "Kirkham C.L."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/name | "J Innate Immun"xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/pages | "584-600"xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/title | "Modulation of Clr Ligand Expression and NKR-P1 Receptor Function during Murine Cytomegalovirus Infection."xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://purl.uniprot.org/core/volume | "7"xsd:string |
| http://purl.uniprot.org/citations/26044139 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26044139 |
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| http://purl.uniprot.org/uniprot/#_G3UZI0-mappedCitation-26044139 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26044139 |
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| http://purl.uniprot.org/uniprot/#_Q64228-mappedCitation-26044139 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26044139 |