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http://purl.uniprot.org/citations/19135240http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19135240http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19135240http://www.w3.org/2000/01/rdf-schema#comment"Dysfunction and loss of insulin-producing pancreatic beta cells represent hallmarks of diabetes mellitus. Here, we show that mice lacking the mitogen-activated protein kinase (MAPK) p38delta display improved glucose tolerance due to enhanced insulin secretion from pancreatic beta cells. Deletion of p38delta results in pronounced activation of protein kinase D (PKD), the latter of which we have identified as a pivotal regulator of stimulated insulin exocytosis. p38delta catalyzes an inhibitory phosphorylation of PKD1, thereby attenuating stimulated insulin secretion. In addition, p38delta null mice are protected against high-fat-feeding-induced insulin resistance and oxidative stress-mediated beta cell failure. Inhibition of PKD1 reverses enhanced insulin secretion from p38delta-deficient islets and glucose tolerance in p38delta null mice as well as their susceptibility to oxidative stress. In conclusion, the p38delta-PKD pathway integrates regulation of the insulin secretory capacity and survival of pancreatic beta cells, pointing to a pivotal role for this pathway in the development of overt diabetes mellitus."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2008.11.018"xsd:string
http://purl.uniprot.org/citations/19135240http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2008.11.018"xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Aebersold R."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Aebersold R."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Bodenmiller B."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Bodenmiller B."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Jiang H."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Jiang H."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Collins S."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Collins S."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Platt K.A."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Platt K.A."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Formentini I."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Formentini I."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Ricci R."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Ricci R."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Sumara G."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Sumara G."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Sumara I."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Sumara I."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Caille D."xsd:string
http://purl.uniprot.org/citations/19135240http://purl.uniprot.org/core/author"Caille D."xsd:string