| http://purl.uniprot.org/citations/10848577 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10848577 | http://www.w3.org/2000/01/rdf-schema#comment | "Activated tumor necrosis factor alpha (TNF-alpha) receptor 1 (TNFR1) recruits TNFR1-associated death domain protein (TRADD), which in turn triggers two opposite signaling pathways leading to caspase activation for apoptosis induction and NF-kappaB activation for antiapoptosis gene upregulation. Here we show that Stat1 is involved in the TNFR1-TRADD signaling complex, as determined by employing a novel antibody array screening method. In HeLa cells, Stat1 was associated with TNFR1 and this association was increased with TNF-alpha treatment. TNFR1 signaling factors TRADD and Fas-associated death domain protein (FADD) were also found to interact with Stat1 in a TNF-alpha-dependent process. Our in vitro recombinant protein-protein interaction studies demonstrated that Stat1 could directly interact with TNFR1 and TRADD but not with FADD. Interaction between Stat1 and receptor-interacting protein (RIP) or TNFR-associated factor 2 (TRAF2) was not detected. Examination of Stat1-deficient cells showed an apparent increase in TNF-alpha-induced TRADD-RIP and TRADD-TRAF2 complex formation, while interaction between TRADD and FADD was unaffected. As a consequence, TNF-alpha-mediated I-kappaB degradation and NF-kappaB activation were markedly enhanced in Stat1-deficient cells, whereas overexpression of Stat1 in 293T cells blocked NF-kappaB activation by TNF-alpha. Thus, Stat1 acts as a TNFR1-signaling molecule to suppress NF-kappaB activation."xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.20.13.4505-4512.2000"xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/author | "Cai S."xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/author | "Chin Y.E."xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/author | "Welte T."xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/author | "Wu T.R."xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/date | "2000"xsd:gYear |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/name | "Mol Cell Biol"xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/pages | "4505-4512"xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/title | "Stat1 as a component of tumor necrosis factor alpha receptor 1-TRADD signaling complex to inhibit NF-kappaB activation."xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://purl.uniprot.org/core/volume | "20"xsd:string |
| http://purl.uniprot.org/citations/10848577 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/10848577 |
| http://purl.uniprot.org/citations/10848577 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/10848577 |
| http://purl.uniprot.org/uniprot/P42224#attribution-45A4BEFA3AE2A958EE5FE9035F3D90CA | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/10848577 |
| http://purl.uniprot.org/uniprot/P42224#attribution-7C7B3A89A44088C588FC6E6E1C1B1278 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/10848577 |
| http://purl.uniprot.org/uniprot/P42224#attribution-E9FA53B49BE54EF30DA879B0A096EE2E | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/10848577 |