| http://purl.uniprot.org/citations/27739494 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27739494 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27739494 | http://www.w3.org/2000/01/rdf-schema#comment | "Insulin receptor substrates (IRSs) are major targets of insulin receptor tyrosine kinases. Here we identified diacylglycerol kinase zeta (DGKζ) as an IRS-1-associated protein, and examined roles of DGKζ in glucose transporter 4 (GLUT4) translocation to the plasma membrane. When DGKζ was knocked-down in 3T3-L1 adipocytes, insulin-induced GLUT4 translocation was inhibited without affecting other mediators of insulin-dependent signaling. Similarly, knockdown of phosphatidylinositol 4-phosphate 5-kinase 1α (PIP5K1α), which had been reported to interact with DGKζ, also inhibited insulin-induced GLUT4 translocation. Moreover, DGKζ interacted with IRS-1 without insulin stimulation, but insulin stimulation decreased this interaction. Over-expression of sDGKζ (short-form DGKζ), which competed out DGKζ from IRS-1, enhanced GLUT4 translocation without insulin stimulation. Taking these results together with the data showing that cellular PIP5K activity was correlated with GLUT4 translocation ability, we concluded that IRS-1-associated DGKζ prevents GLUT4 translocation in the absence of insulin and that the DGKζ dissociated from IRS-1 by insulin stimulation enhances GLUT4 translocation through PIP5K1α activity."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.org/dc/terms/identifier | "doi:10.1038/srep35438"xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.org/dc/terms/identifier | "doi:10.1038/srep35438"xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Liu T."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Liu T."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Yu B."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Yu B."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Fujimoto H."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Fujimoto H."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Ando Y."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Ando Y."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Hakuno F."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Hakuno F."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Kakino M."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Kakino M."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Takahashi S.I."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/author | "Takahashi S.I."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/name | "Sci. Rep."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/name | "Sci. Rep."xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/pages | "35438"xsd:string |
| http://purl.uniprot.org/citations/27739494 | http://purl.uniprot.org/core/pages | "35438"xsd:string |