{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["283(36)"],"submitter":["Varfolomeev E"],"pubmed_abstract":["The inhibitor of apoptosis (IAP) proteins are a family of anti-apoptotic regulators found in viruses and metazoans. c-IAP1 and c-IAP2 are recruited to tumor necrosis factor receptor 1 (TNFR1)-associated complexes where they can regulate receptor-mediated signaling. Both c-IAP1 and c-IAP2 have been implicated in TNFalpha-stimulated NF-kappaB activation. However, individual c-IAP1 and c-IAP2 gene knock-outs in mice did not reveal changes in TNF signaling pathways, and the phenotype of a combined deficiency of c-IAPs has yet to be reported. Here we investigate the role of c-IAP1 and c-IAP2 in TNFalpha-stimulated activation of NF-kappaB. We demonstrate that TNFalpha-induced NF-kappaB activation is severely diminished in the absence of both c-IAP proteins. In addition, combined absence of c-IAP"],"journal":["The Journal of biological chemistry"],"pagination":["24295-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3259840"],"repository":["biostudies-literature"],"pubmed_title":["c-IAP1 and c-IAP2 are critical mediators of tumor necrosis factor alpha (TNFalpha)-induced NF-kappaB activation."],"pmcid":["PMC3259840"],"pubmed_authors":["Zobel K","Fairbrother WJ","Vucic D","Dynek JN","Deshayes K","Varfolomeev E","Goncharov T","Fedorova AV"],"additional_accession":[]},"is_claimable":false,"name":"c-IAP1 and c-IAP2 are critical mediators of tumor necrosis factor alpha (TNFalpha)-induced NF-kappaB activation.","description":"The inhibitor of apoptosis (IAP) proteins are a family of anti-apoptotic regulators found in viruses and metazoans. c-IAP1 and c-IAP2 are recruited to tumor necrosis factor receptor 1 (TNFR1)-associated complexes where they can regulate receptor-mediated signaling. Both c-IAP1 and c-IAP2 have been implicated in TNFalpha-stimulated NF-kappaB activation. However, individual c-IAP1 and c-IAP2 gene knock-outs in mice did not reveal changes in TNF signaling pathways, and the phenotype of a combined deficiency of c-IAPs has yet to be reported. Here we investigate the role of c-IAP1 and c-IAP2 in TNFalpha-stimulated activation of NF-kappaB. We demonstrate that TNFalpha-induced NF-kappaB activation is severely diminished in the absence of both c-IAP proteins. In addition, combined absence of c-IAP","dates":{"release":"2008-01-01T00:00:00Z","publication":"2008 Sep","modification":"2025-04-26T16:53:37.926Z","creation":"2019-03-27T00:48:03Z"},"accession":"S-EPMC3259840","cross_references":{"pubmed":["18621737"],"doi":["10.1074/jbc.C800128200","10.1074/jbc.c800128200"]}}