| http://purl.uniprot.org/citations/12881524 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12881524 | http://www.w3.org/2000/01/rdf-schema#comment | "The human insulin receptor (IR) exists in two isoforms (IR-A and IR-B). IR-A is a short isoform, generated by the skipping of exon 11, a small exon encoding for 12 amino acid residues at the carboxyl terminus of the IR alpha-subunit. Recently, we found that IR-A is the predominant isoform in fetal tissues and malignant cells and binds with a high affinity not only insulin but also insulin-like growth factor-II (IGF-II). To investigate whether the activation of IR-A by the two ligands differentially activate post-receptor molecular mechanisms, we studied gene expression in response to IR-A activation by either insulin or IGF-II, using microarray technology. To avoid the interfering effect of the IGF-IR, IGF-II binding to the IR-A was studied in IGF-IR-deficient murine fibroblasts (R-cells) transfected with the human IR-A cDNA (R-/IR-A cells). Gene expression was studied at 0.5, 3, and 8 h. We found that 214 transcripts were similarly regulated by insulin and IGF-II, whereas 45 genes were differentially transcribed. Eighteen of these differentially regulated genes were responsive to only one of the two ligands (12 to insulin and 6 to IGF-II). Twenty-seven transcripts were regulated by both insulin and IGF-II, but a significant difference between the two ligands was present at least in one time point. Interestingly, IGF-II was a more potent and/or persistent regulator than insulin for these genes. Results were validated by measuring the expression of 12 genes by quantitative real-time reverse transcriptase-PCR. In conclusion, we show that insulin and IGF-II, acting via the same receptor, may differentially affect gene expression in cells. These studies provide a molecular basis for understanding some of the biological differences between the two ligands and may help to clarify the biological role of IR-A in embryonic/fetal growth and the selective biological advantage that malignant cells producing IGF-II may acquire via IR-A overexpression."xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m304980200"xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/author | "Belfiore A."xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/author | "Vigneri R."xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/author | "Pandini G."xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/author | "Sciacca L."xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/author | "Conte E."xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/author | "Medico E."xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/pages | "42178-42189"xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/title | "Differential gene expression induced by insulin and insulin-like growth factor-II through the insulin receptor isoform A."xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://purl.uniprot.org/core/volume | "278"xsd:string |
| http://purl.uniprot.org/citations/12881524 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/12881524 |
| http://purl.uniprot.org/citations/12881524 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/12881524 |
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