| http://purl.uniprot.org/citations/24337384 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24337384 | http://www.w3.org/2000/01/rdf-schema#comment | "The endosomal innate receptor CD158d (killer cell Ig-like receptor 2DL4) induces cellular senescence in human NK cells in response to soluble ligand (HLA-G or agonist Ab). These senescent NK cells display a senescence-associated secretory phenotype, and their secretome promotes vascular remodeling and angiogenesis. To understand how CD158d initiates signaling for a senescence response, we mapped the region in its cytoplasmic tail that controls signaling. We identified a conserved TNFR-associated factor 6 (TRAF6) binding motif, which was required for CD158d-induced NF-κB activation and IL-8 secretion, TRAF6 association with CD158d, and TRAF6 recruitment to CD158d(+) endosomes in transfected cells. The adaptor TRAF6 is known to couple proximal signals from receptors such as endosomal TLRs and CD40 through the kinase TGF-β-activated kinase 1 (TAK1) for NF-κB-dependent proinflammatory responses. Small interfering RNA-mediated silencing of TRAF6 and TAK1, and inhibition of TAK1 blocked CD158d-dependent IL-8 secretion. Stimulation of primary, resting NK cells with soluble Ab to CD158d induced TRAF6 association with CD158d, induced TAK1 phosphorylation, and inhibition of TAK1 blocked the CD158d-dependent reprogramming of NK cells that produces the senescence-associated secretory phenotype signature. Our results reveal that a prototypic TLR and TNFR signaling pathway is used by a killer cell Ig-like receptor that promotes secretion of proinflammatory and proangiogenic mediators as part of a unique senescence phenotype in NK cells."xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1302384"xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://purl.uniprot.org/core/author | "Rajagopalan S."xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://purl.uniprot.org/core/author | "Lee E.C."xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://purl.uniprot.org/core/author | "Long E.O."xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://purl.uniprot.org/core/author | "DuPrie M.L."xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24337384 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://purl.uniprot.org/core/pages | "714-721"xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://purl.uniprot.org/core/title | "TNFR-associated factor 6 and TGF-beta-activated kinase 1 control signals for a senescence response by an endosomal NK cell receptor."xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://purl.uniprot.org/core/volume | "192"xsd:string |
| http://purl.uniprot.org/citations/24337384 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24337384 |
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