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http://purl.uniprot.org/citations/25586176http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25586176http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25586176http://www.w3.org/2000/01/rdf-schema#comment"Insulin receptor substrates (IRSs) have been shown to be major mediators of insulin signaling. Recently, we found that IRSs form high-molecular weight complexes, and here, we identify by yeast two-hybrid screening a novel IRS-1-associated protein: a 42-kDa cGMP-dependent protein kinase-anchoring protein (GKAP42). GKAP42 knockdown in 3T3-L1 adipocytes suppressed insulin-dependent IRS-1 tyrosine phosphorylation and downstream signaling, resulting in suppression of GLUT4 translocation to plasma membrane induced by insulin. In addition, GLUT4 translocation was also suppressed in cells overexpressing GKAP42-N (the IRS-1 binding region of GKAP42), which competed with GKAP42 for IRS-1, indicating that GKAP42 binding to IRS-1 is required for insulin-induced GLUT4 translocation. Long term treatment of 3T3-L1 adipocytes with TNF-α, which induced insulin resistance, significantly decreased the GKAP42 protein level. We then investigated the roles of cGMP-dependent kinase (cGK)-Iα, which bound to GKAP42, in these changes. cGK-Iα knockdown partially rescued TNF-α-induced decrease in GKAP42 and impairment of insulin signals. These data indicated that TNF-α-induced repression of GKAP42 via cGK-Iα caused reduction of insulin-induced IRS-1 tyrosine phosphorylation at least in part. The present study describes analysis of the novel TNF-α-induced pathway, cGK-Iα-GKAP42, which regulates insulin-dependent signals and GLUT4 translocation."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m114.624759"xsd:string
http://purl.uniprot.org/citations/25586176http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m114.624759"xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Iijima Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Iijima Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Takahashi S."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Takahashi S."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Ando Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Ando Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Sone M."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Sone M."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Hakuno F."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Hakuno F."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Chida K."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Chida K."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Ooi Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Ooi Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Shinozawa Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Shinozawa Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Watanaka Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Watanaka Y."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Yu B.C."xsd:string
http://purl.uniprot.org/citations/25586176http://purl.uniprot.org/core/author"Yu B.C."xsd:string