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http://purl.uniprot.org/citations/23332762http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23332762http://www.w3.org/2000/01/rdf-schema#comment"The IκB kinase complex (IKK) is a key regulator of immune responses, inflammation, cell survival, and tumorigenesis. The prosurvival function of IKK centers on activation of the transcription factor NF-κB, whose target gene products inhibit caspases and prevent prolonged JNK activation. Here, we report that inactivation of the BH3-only protein BAD by IKK independently of NF-κB activation suppresses TNFα-induced apoptosis. TNFα-treated Ikkβ(-/-) mouse embryonic fibroblasts (MEFs) undergo apoptosis significantly faster than MEFs deficient in both RelA and cRel due to lack of inhibition of BAD by IKK. IKK phosphorylates BAD at serine-26 (Ser26) and primes it for inactivation. Elimination of Ser26 phosphorylation promotes BAD proapoptotic activity, thereby accelerating TNFα-induced apoptosis in cultured cells and increasing mortality in animals. Our results reveal that IKK inhibits TNFα-induced apoptosis through two distinct but cooperative mechanisms: activation of the survival factor NF-κB and inactivation of the proapoptotic BH3-only BAD protein."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2012.12.021"xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Liu J."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Ma J."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Lin Y."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Sun J."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Yan J."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Xiang J."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Lin A."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/author"Danial N.N."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/name"Cell"xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/pages"304-315"xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/title"Inactivation of BAD by IKK inhibits TNFalpha-induced apoptosis independently of NF-kappaB activation."xsd:string
http://purl.uniprot.org/citations/23332762http://purl.uniprot.org/core/volume"152"xsd:string
http://purl.uniprot.org/citations/23332762http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23332762
http://purl.uniprot.org/citations/23332762http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23332762
http://purl.uniprot.org/uniprot/#_A0A0R4J0T4-mappedCitation-23332762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23332762
http://purl.uniprot.org/uniprot/#_Q0X0E6-mappedCitation-23332762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23332762
http://purl.uniprot.org/uniprot/#_A0A0R4J210-mappedCitation-23332762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23332762
http://purl.uniprot.org/uniprot/#_A4L9Q2-mappedCitation-23332762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23332762
http://purl.uniprot.org/uniprot/#_A0A494B901-mappedCitation-23332762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23332762