| http://purl.uniprot.org/citations/21525013 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21525013 | http://www.w3.org/2000/01/rdf-schema#comment | "The tumor necrosis factor (TNF) superfamily member TNF-like weak inducer of apoptosis (TNFSF12, CD255) (TWEAK) can stimulate apoptosis in certain cancer cells. Previous studies suggest that TWEAK activates cell death indirectly, by inducing TNFα-mediated autocrine signals. However, the underlying death-signaling mechanism has not been directly defined. Consistent with earlier work, TWEAK assembled a proximal signaling complex containing its cognate receptor FN14, the adaptor TRAF2, and cellular inhibitor of apoptosis protein 1 (cIAP1). Neither the death domain adaptor Fas-associated death domain nor the apoptosis-initiating protease caspase-8 associated with this primary complex. Rather, TWEAK induced TNFα secretion and TNF receptor 1-dependent assembly of a death-signaling complex containing receptor-interacting protein 1 (RIP1), FADD, and caspase-8. Knockdown of RIP1 by siRNA prevented TWEAK-induced association of FADD with caspase-8 but not formation of the FN14-TRAF2-cIAP1 complex and inhibited apoptosis activation. Depletion of the RIP1 E3 ubiquitin ligase cIAP1 enhanced assembly of the RIP1-FADD-caspase-8 complex and augmented cell death. Conversely, knockdown of the RIP1 deubiquitinase CYLD inhibited these functions. Depletion of FADD, caspase-8, BID, or BAX and BAK but not RIP3 attenuated TWEAK-induced cell death. Pharmacologic inhibition of the NF-κB pathway or siRNA knockdown of RelA attenuated TWEAK induction of TNFα and association of RIP1 with FADD and caspase-8. These results suggest that TWEAK triggers apoptosis by promoting assembly of a RIP1-FADD-caspse-8 complex via autocrine TNFα-TNFR1 signaling. The proapoptotic activity of TWEAK is modulated by cIAP1 and CYLD and engages both the extrinsic and intrinsic signaling pathways."xsd:string |
| http://purl.uniprot.org/citations/21525013 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m110.203745"xsd:string |
| http://purl.uniprot.org/citations/21525013 | http://purl.uniprot.org/core/author | "Ashkenazi A."xsd:string |
| http://purl.uniprot.org/citations/21525013 | http://purl.uniprot.org/core/author | "Ikner A."xsd:string |
| http://purl.uniprot.org/citations/21525013 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21525013 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/21525013 | http://purl.uniprot.org/core/pages | "21546-21554"xsd:string |
| http://purl.uniprot.org/citations/21525013 | http://purl.uniprot.org/core/title | "TWEAK induces apoptosis through a death-signaling complex comprising receptor-interacting protein 1 (RIP1), Fas-associated death domain (FADD), and caspase-8."xsd:string |
| http://purl.uniprot.org/citations/21525013 | http://purl.uniprot.org/core/volume | "286"xsd:string |
| http://purl.uniprot.org/citations/21525013 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21525013 |
| http://purl.uniprot.org/citations/21525013 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/21525013 |
| http://purl.uniprot.org/uniprot/Q13490#attribution-7D3C4934256B54299751DF7536982DDC | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/Q9NQC7#attribution-ABA835547A93B75A36EFB0CA38870B14 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/Q13158#attribution-ABA835547A93B75A36EFB0CA38870B14 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/Q13546#attribution-ABA835547A93B75A36EFB0CA38870B14 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/O43508#attribution-7D3C4934256B54299751DF7536982DDC | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/Q9NP84#attribution-7D3C4934256B54299751DF7536982DDC | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/Q9NP84#attribution-ABA835547A93B75A36EFB0CA38870B14 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/Q12933#attribution-ABA835547A93B75A36EFB0CA38870B14 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/#_A0A0U5J5F5-mappedCitation-21525013 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/#_B3KU53-mappedCitation-21525013 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/#_B4DDS8-mappedCitation-21525013 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/#_C0H5Y4-mappedCitation-21525013 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21525013 |
| http://purl.uniprot.org/uniprot/#_Q13158-mappedCitation-21525013 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21525013 |