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http://purl.uniprot.org/citations/23524849http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23524849http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23524849http://www.w3.org/2000/01/rdf-schema#comment"The cellular inhibitor of apoptosis (c-IAP) proteins are E3 ubiquitin ligases that are critical regulators of tumour necrosis factor (TNF) receptor (TNFR)-mediated signalling. Through their E3 ligase activity c-IAP proteins promote ubiquitination of receptor-interaction protein 1 (RIP1), NF-κB-inducing kinase (NIK) and themselves, and regulate the assembly of TNFR signalling complexes. Consequently, in the absence of c-IAP proteins, TNFR-mediated activation of NF-κB and MAPK pathways and the induction of gene expression are severely reduced. Here, we describe the identification of OTUB1 as a c-IAP-associated deubiquitinating enzyme that regulates c-IAP1 stability. OTUB1 disassembles K48-linked polyubiquitin chains from c-IAP1 in vitro and in vivo within the TWEAK receptor-signalling complex. Downregulation of OTUB1 promotes TWEAK- and IAP antagonist-stimulated caspase activation and cell death, and enhances c-IAP1 degradation. Furthermore, knockdown of OTUB1 reduces TWEAK-induced activation of canonical NF-κB and MAPK signalling pathways and modulates TWEAK-induced gene expression. Finally, suppression of OTUB1 expression in zebrafish destabilizes c-IAP (Birc2) protein levels and disrupts fish vasculature. These results suggest that OTUB1 regulates NF-κB and MAPK signalling pathways and TNF-dependent cell death by modulating c-IAP1 stability."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.org/dc/terms/identifier"doi:10.1038/emboj.2013.62"xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Kirkpatrick D.S."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Kirkpatrick D.S."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Vucic D."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Vucic D."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Arnott D."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Arnott D."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Izrael-Tomasevic A."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Izrael-Tomasevic A."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Deshayes K."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Deshayes K."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Fedorova A.V."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Fedorova A.V."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Goncharov T."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Goncharov T."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Varfolomeev E."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Varfolomeev E."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"de Almagro M.C."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"de Almagro M.C."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Niessen K."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/author"Niessen K."xsd:string
http://purl.uniprot.org/citations/23524849http://purl.uniprot.org/core/date"2013"xsd:gYear