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http://purl.uniprot.org/citations/22264792http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22264792http://www.w3.org/2000/01/rdf-schema#comment"Constitutive Kras and NF-κB activation is identified as signature alterations in pancreatic ductal adenocarcinoma (PDAC). However, how NF-κB is activated in PDAC is not yet understood. Here, we report that pancreas-targeted IKK2/β inactivation inhibited NF-κB activation and PDAC development in Kras(G12D) and Kras(G12D);Ink4a/Arf(F/F) mice, demonstrating a mechanistic link between IKK2/β and Kras(G12D) in PDAC inception. Our findings reveal that Kras(G12D)-activated AP-1 induces IL-1α, which, in turn, activates NF-κB and its target genes IL-1α and p62, to initiate IL-1α/p62 feedforward loops for inducing and sustaining NF-κB activity. Furthermore, IL-1α overexpression correlates with Kras mutation, NF-κB activity, and poor survival in PDAC patients. Therefore, our findings demonstrate the mechanism by which IKK2/β/NF-κB is activated by Kras(G12D) through dual feedforward loops of IL-1α/p62."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.org/dc/terms/identifier"doi:10.1016/j.ccr.2011.12.006"xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Liu J."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Ling J."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Kang Y."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Wang H."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Zhao R."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Xia Q."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Chang Z."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Hung M.C."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Lemischka I.R."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Peng B."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Lee D.F."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Chiao P.J."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/author"Fleming J.B."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/name"Cancer Cell"xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/pages"105-120"xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/title"KrasG12D-induced IKK2/beta/NF-kappaB activation by IL-1alpha and p62 feedforward loops is required for development of pancreatic ductal adenocarcinoma."xsd:string
http://purl.uniprot.org/citations/22264792http://purl.uniprot.org/core/volume"21"xsd:string
http://purl.uniprot.org/citations/22264792http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22264792
http://purl.uniprot.org/citations/22264792http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22264792
http://purl.uniprot.org/uniprot/#_A0A0R4J0T4-mappedCitation-22264792http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22264792