{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362825894065254144.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1126/science.1106148"}},{"identifier":{"@type":"URI","@value":"https://www.science.org/doi/pdf/10.1126/science.1106148"}},{"identifier":{"@type":"NAID","@value":"80017253279"}}],"dc:title":[{"@value":"Phosphorylation and Regulation of Akt/PKB by the Rictor-mTOR Complex"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>\n                    Deregulation of Akt/protein kinase B (PKB) is implicated in the pathogenesis of cancer and diabetes. Akt/PKB activation requires the phosphorylation of Thr\n                    <jats:sup>308</jats:sup>\n                    in the activation loop by the phosphoinositide-dependent kinase 1 (PDK1) and Ser\n                    <jats:sup>473</jats:sup>\n                    within the carboxyl-terminal hydrophobic motif by an unknown kinase. We show that in\n                    <jats:italic>Drosophila</jats:italic>\n                    and human cells the target of rapamycin (TOR) kinase and its associated protein rictor are necessary for Ser\n                    <jats:sup>473</jats:sup>\n                    phosphorylation and that a reduction in rictor or mammalian TOR (mTOR) expression inhibited an Akt/PKB effector. The rictor-mTOR complex directly phosphorylated Akt/PKB on Ser\n                    <jats:sup>473</jats:sup>\n                    in vitro and facilitated Thr\n                    <jats:sup>308</jats:sup>\n                    phosphorylation by PDK1. Rictor-mTOR may serve as a drug target in tumors that have lost the expression of PTEN, a tumor suppressor that opposes Akt/PKB activation.\n                  </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382825894065254144","@type":"Researcher","foaf:name":[{"@value":"Dos D. Sarbassov"}],"jpcoar:affiliationName":[{"@value":"Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA. Broad Institute, 320 Charles Street, Cambridge, MA 02141, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894065254146","@type":"Researcher","foaf:name":[{"@value":"David A. Guertin"}],"jpcoar:affiliationName":[{"@value":"Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA. Broad Institute, 320 Charles Street, Cambridge, MA 02141, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894065254147","@type":"Researcher","foaf:name":[{"@value":"Siraj M. Ali"}],"jpcoar:affiliationName":[{"@value":"Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA. Broad Institute, 320 Charles Street, Cambridge, MA 02141, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894065254145","@type":"Researcher","foaf:name":[{"@value":"David M. Sabatini"}],"jpcoar:affiliationName":[{"@value":"Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA. Broad Institute, 320 Charles Street, Cambridge, MA 02141, USA."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00368075"},{"@type":"EISSN","@value":"10959203"},{"@type":"PISSN","@value":"http://id.crossref.org/issn/00368075"}],"prism:publicationName":[{"@value":"Science"}],"dc:publisher":[{"@value":"American Association for the Advancement of Science (AAAS)"}],"prism:publicationDate":"2005-02-18","prism:volume":"307","prism:number":"5712","prism:startingPage":"1098","prism:endingPage":"1101"},"reviewed":"false","url":[{"@id":"https://www.science.org/doi/pdf/10.1126/science.1106148"}],"createdAt":"2005-02-17","modifiedAt":"2024-01-09","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050001202611267840","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"mTOR plays critical roles in pancreatic cancer stem cells through specific and stemness-related 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