| http://purl.uniprot.org/citations/33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/33126536 | http://www.w3.org/2000/01/rdf-schema#comment | "Cytomegaloviruses all encode the viral inhibitor of caspase-8-induced apoptosis (vICA). After binding to this initiator caspase, vICA blocks caspase-8 proteolytic activity and ability to activate caspase-3 and/or caspase-7. In this manner, vICA has long been known to prevent apoptosis triggered via tumor necrosis factor (TNF) family death receptor-dependent extrinsic signaling. Here, we employ fully wild-type murine cytomegalovirus (MCMV) and vICA-deficient MCMV (∆M36) to investigate the contribution of TNF signaling to apoptosis during infection of different cell types. ∆M36 shows the expected ability to kill mouse splenic hematopoietic cells, bone marrow-derived macrophages (BMDM), and dendritic cells (BMDC). Antibody blockade or genetic elimination of TNF protects myeloid cells from death, and caspase-8 activation accompanies cell death. Interferons, necroptosis, and pyroptotic gasdermin D (GSDMD) do not contribute to myeloid cell death. Human and murine fibroblasts or murine endothelial cells (SVEC4-10) normally insensitive to TNF become sensitized to ∆M36-induced apoptosis when treated with TNF or TNF-containing BMDM-conditioned medium. We demonstrate that myeloid cells are the natural source of TNF that triggers apoptosis in either myeloid (autocrine) or non-myeloid cells (paracrine) during ∆M36 infection of mice. Caspase-8 suppression by vICA emerges as key to subverting innate immune elimination of a wide variety of infected cell types."xsd:string |
| http://purl.uniprot.org/citations/33126536 | http://purl.org/dc/terms/identifier | "doi:10.3390/v12111221"xsd:string |
| http://purl.uniprot.org/citations/33126536 | http://purl.uniprot.org/core/author | "Mocarski E.S."xsd:string |
| http://purl.uniprot.org/citations/33126536 | http://purl.uniprot.org/core/author | "Mandal P."xsd:string |
| http://purl.uniprot.org/citations/33126536 | http://purl.uniprot.org/core/author | "McCormick A.L."xsd:string |
| http://purl.uniprot.org/citations/33126536 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/33126536 | http://purl.uniprot.org/core/name | "Viruses"xsd:string |
| http://purl.uniprot.org/citations/33126536 | http://purl.uniprot.org/core/pages | "E1221"xsd:string |
| http://purl.uniprot.org/citations/33126536 | http://purl.uniprot.org/core/title | "TNF Signaling Dictates Myeloid and Non-Myeloid Cell Crosstalk to Execute MCMV-Induced Extrinsic Apoptosis."xsd:string |
| http://purl.uniprot.org/citations/33126536 | http://purl.uniprot.org/core/volume | "12"xsd:string |
| http://purl.uniprot.org/citations/33126536 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/33126536 |
| http://purl.uniprot.org/citations/33126536 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/33126536 |
| http://purl.uniprot.org/uniprot/#_A0A087WQT6-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_E9PZP3-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_Q0X0E6-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_A0A0R4J210-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_A0A0U5J4W4-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_A0A2I3BPT3-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_A0A338P6T9-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_A0A338P6X7-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_A0A384DVB8-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_A0A2I3BQW9-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_E9PWM1-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |
| http://purl.uniprot.org/uniprot/#_Q3U593-mappedCitation-33126536 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33126536 |