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http://purl.uniprot.org/citations/20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20555424http://www.w3.org/2000/01/rdf-schema#comment"Cardiovascular disease involves changes in inflammatory markers. Since insulin/insulin-like growth factor 1 receptor (IGF-1R) can activate vascular endothelial growth factor to promote vascular growth, reduced IGF-1R signaling in the type I diabetic heart could be detrimental, leading to reduced, collateral blood vessel growth. This study assessed whether diabetes can induce an inflammatory phenotype to regulate molecules in the IGF-1 signaling cascade, thus mediating apoptosis. Rats were made diabetic using streptozotocin (to render them type I diabetic) for 2 months with no insulin treatment. At 2 months, rats were sacrificed under anesthesia, and the left ventricle was immediately removed and placed into cold lysis buffer for protein analyses. Western blotting, immunoprecipitation, and enzyme-linked immunosorbent assay analyses were completed to evaluate protein levels. Diabetes increased TNF-alpha, interleukin-6 (IL-6), and IL-1alpha levels in the heart. JNK and p42/p44 activity was significantly increased in the diabetic heart, while IGF-1R phosphorylation, IRS-2 tyrosine phosphorylation, and Akt activities were reduced. A significant increase in Bad protein levels and the cleavage of caspase 3 was observed in the diabetic heart. These results suggest that diabetes activates multiple inflammatory markers in the heart, which then signal a decrease in the activities of key players in the insulin-signaling cascade, namely IGF-1R, IRS-2, and Akt, to regulate apoptosis."xsd:string
http://purl.uniprot.org/citations/20555424http://purl.org/dc/terms/identifier"doi:10.1139/y10-006"xsd:string
http://purl.uniprot.org/citations/20555424http://purl.uniprot.org/core/author"Jiang Y."xsd:string
http://purl.uniprot.org/citations/20555424http://purl.uniprot.org/core/author"Steinle J.J."xsd:string
http://purl.uniprot.org/citations/20555424http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20555424http://purl.uniprot.org/core/name"Can J Physiol Pharmacol"xsd:string
http://purl.uniprot.org/citations/20555424http://purl.uniprot.org/core/pages"553-561"xsd:string
http://purl.uniprot.org/citations/20555424http://purl.uniprot.org/core/title"Regulation of IRS-2 signaling by IGF-1 receptor in the diabetic rat heart."xsd:string
http://purl.uniprot.org/citations/20555424http://purl.uniprot.org/core/volume"88"xsd:string
http://purl.uniprot.org/citations/20555424http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20555424
http://purl.uniprot.org/citations/20555424http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/20555424
http://purl.uniprot.org/uniprot/#_A0A0G2JX40-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_A0A0G2K003-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_A0A140TAB8-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_A0A8L2UL72-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_A0A8L2URC2-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_A0A8I6A641-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_A0A8I6AGT8-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_F1MAL5-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_F1LQB1-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_F8WFZ5-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_P24062-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_P16598-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424
http://purl.uniprot.org/uniprot/#_P16599-mappedCitation-20555424http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20555424