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http://purl.uniprot.org/citations/17596282http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17596282http://www.w3.org/2000/01/rdf-schema#comment"beta-catenin signaling is heavily involved in organogenesis. Here, we investigated how pancreas differentiation, growth and homeostasis are affected following inactivation of an endogenous inhibitor of beta-catenin, adenomatous polyposis coli (Apc). In adult mice, Apc-deficient pancreata were enlarged, solely as a result of hyperplasia of acinar cells, which accumulated beta-catenin, with the sparing of islets. Expression of a target of beta-catenin, the proto-oncogene c-myc (Myc), was increased in acinar cells lacking Apc, suggesting that c-myc expression is essential for hyperplasia. In support of this hypothesis, we found that conditional inactivation of c-myc in pancreata lacking Apc completely reversed the acinar hyperplasia. Apc loss in organs such as the liver, colon and kidney, as well as experimental misexpression of c-myc in pancreatic acinar cells, led to tumor formation with high penetrance. Surprisingly, pancreas tumors failed to develop following conditional pancreas Apc inactivation. In Apc-deficient acini of aged mice, our studies revealed a cessation of their exaggerated proliferation and a reduced expression of c-myc, in spite of the persistent accumulation of beta-catenin. In conclusion, our work shows that beta-catenin modulation of c-myc is an essential regulator of acinar growth control, and unveils an unprecedented example of Apc requirement in the pancreas that is both temporally restricted and cell-specific. This provides new insights into the mechanisms of tumor pathogenesis and tumor suppression in the pancreas."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.org/dc/terms/identifier"doi:10.1242/dev.02875"xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Kido Y."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Hashimoto N."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Noda T."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Campos M.L."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Real F.X."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Thorel F."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Ashery-Padan R."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Trumpp A."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Herrera P.L."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Strom A."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/author"Bonal C."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/name"Development"xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/pages"2719-2725"xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/title"Unique mechanisms of growth regulation and tumor suppression upon Apc inactivation in the pancreas."xsd:string
http://purl.uniprot.org/citations/17596282http://purl.uniprot.org/core/volume"134"xsd:string
http://purl.uniprot.org/citations/17596282http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17596282
http://purl.uniprot.org/citations/17596282http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17596282
http://purl.uniprot.org/uniprot/Q61315#attribution-62198A84910ECDD872A0D988CACF30F5http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17596282
http://purl.uniprot.org/uniprot/P01108#attribution-5FF66D05137D7DB986E19B50AE29D0E6http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17596282
http://purl.uniprot.org/uniprot/#_D3Z7S6-mappedCitation-17596282http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17596282
http://purl.uniprot.org/uniprot/#_A0A0J9YU51-mappedCitation-17596282http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17596282