| http://purl.uniprot.org/citations/19233842 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19233842 | http://www.w3.org/2000/01/rdf-schema#comment | "Therapeutics based on the actions of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), have recently been introduced for the treatment of type 2 diabetes mellitus. The serine/threonine kinase Akt is a major mediator of incretin action on the pancreatic islet, increasing beta-cell mass and function and promoting beta-cell survival. The mechanisms underlying incretin activation of Akt are thought to involve an essential phosphoinositide 3-kinase-mediated phosphorylation of threonine 308, similar to the prototypical Akt activator, insulin-like growth factor-I (IGF-I). In this study, using activity assays on immunoprecipitated Akt, we discovered that GIP and GLP-1 were capable of stimulating Akt in the INS-1 beta-cell line and isolated mouse islets via a mechanism that did not require phosphoinositide 3-kinase or phosphorylation of Thr(308) and Ser(473), and this pathway involved the production of cAMP. Furthermore, we found that GIP stimulated anti-apoptotic signaling via this alternate mode of Akt activation. We conclude that incretins can activate Akt via a novel noncanonical mechanism that may provide an alternative therapeutic target for the treatment of type 2 diabetes mellitus and have broader implications for Akt physiology in human health and disease."xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m809116200"xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://purl.uniprot.org/core/author | "Underhill T.M."xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://purl.uniprot.org/core/author | "McIntosh C.H."xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://purl.uniprot.org/core/author | "Widenmaier S.B."xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://purl.uniprot.org/core/author | "Sampaio A.V."xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19233842 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://purl.uniprot.org/core/pages | "10764-10773"xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://purl.uniprot.org/core/title | "Noncanonical activation of Akt/protein kinase B in {beta}-cells by the incretin hormone glucose-dependent insulinotropic polypeptide."xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://purl.uniprot.org/core/volume | "284"xsd:string |
| http://purl.uniprot.org/citations/19233842 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19233842 |
| http://purl.uniprot.org/citations/19233842 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19233842 |
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| http://purl.uniprot.org/uniprot/#_A6HIC4-mappedCitation-19233842 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19233842 |
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