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http://purl.uniprot.org/citations/16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16984735http://www.w3.org/2000/01/rdf-schema#comment"Neurotensin (NT), a gastrointestinal hormone, binds its receptor [neurotensin receptor (NTR)] to regulate the growth of normal and neoplastic intestinal cells; molecular mechanisms remain largely undefined. Glycogen synthase kinase-3 (GSK-3) regulates diverse cellular processes, including cell growth and apoptosis. Here, we show that NT induces the phosphorylation of GSK-3alpha/beta in the human colon cancer cell line HT29, HCT116, or SW480, which possesses high-affinity NTR. The effect of NT was blocked by inhibitors of protein kinase C (PKC), but not by inhibitors of MEK1 or phosphatidylinositol-3 kinase, suggesting a predominant role for PKC in GSK-3beta phosphorylation by NT. Pretreatment with Gö6976 (which inhibits PKCalpha and PKCbeta1) or downregulation of endogenous PKCalpha or PKCbeta1 blocked NT-mediated GSK-3beta (but not GSK-3alpha) phosphorylation. Moreover, a selective PKCbeta inhibitor, LY379196, reduced NT-mediated GSK-3beta (but not GSK-3alpha) phosphorylation, suggesting a role for PKCbeta1 in the NT-mediated phosphorylation of GSK-3beta and an undefined kinase in the NT-mediated phosphorylation of GSK-3alpha. Treatment with NT or the GSK-3 inhibitor SB216763 increased the expression of cyclin D1, a downstream effector protein of GSK-3 and a critical protein for the proliferation of various cells. Our results indicate that NT uses PKC-dependent pathways to modulate GSK-3, which may play a role in the NT regulation of intestinal cell growth."xsd:string
http://purl.uniprot.org/citations/16984735http://purl.org/dc/terms/identifier"doi:10.1593/neo.06259"xsd:string
http://purl.uniprot.org/citations/16984735http://purl.uniprot.org/core/author"Wang Q."xsd:string
http://purl.uniprot.org/citations/16984735http://purl.uniprot.org/core/author"Zhou Y."xsd:string
http://purl.uniprot.org/citations/16984735http://purl.uniprot.org/core/author"Evers B.M."xsd:string
http://purl.uniprot.org/citations/16984735http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16984735http://purl.uniprot.org/core/name"Neoplasia"xsd:string
http://purl.uniprot.org/citations/16984735http://purl.uniprot.org/core/pages"781-787"xsd:string
http://purl.uniprot.org/citations/16984735http://purl.uniprot.org/core/title"Neurotensin phosphorylates GSK-3alpha/beta through the activation of PKC in human colon cancer cells."xsd:string
http://purl.uniprot.org/citations/16984735http://purl.uniprot.org/core/volume"8"xsd:string
http://purl.uniprot.org/citations/16984735http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16984735
http://purl.uniprot.org/citations/16984735http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16984735
http://purl.uniprot.org/uniprot/#_A0A3B3ITW1-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_A0A169TED2-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_B0LPH5-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_B5BUC0-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_G3V1X6-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_P49840-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_P49841-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_Q7Z727-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_L7RSM7-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_Q86TM2-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_Q86U50-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735
http://purl.uniprot.org/uniprot/#_P17252-mappedCitation-16984735http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16984735