http://purl.uniprot.org/citations/17102589 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/17102589 | http://www.w3.org/2000/01/rdf-schema#comment | "The p53 tumor suppressor induces cellular growth arrest and apoptosis in response to DNA damage by transcriptionally activating or repressing target genes and also through protein-protein interactions and direct mitochondrial activities. In 1995, insulin-like growth factor binding protein (IGFBP)-3 was identified as one of the genes transcriptionally activated by p53. IGFBP-3 is one of six closely related IGFBP's, with additional IGFBP-related proteins belonging to the IGFBP superfamily. Here we show that IGFBP-2 is also a p53 target. Like IGFBP-3, IGFBP-2 secretion is reduced when p53+/+ lung cancer cells are transfected with human papillomavirus E6, which targets p53 for degradation. IGFBP-2 mRNA is induced by irradiation in vivo in a p53-dependent manner. p53 protein binds IGFBP-2 intronic sequences in an electrophoretic mobility shift assay, and activates transcription in a luciferase assay. Loss of IGFBP-2 inhibits the ability of p53 to inhibit the activation of extracellular signal-regulated kinase (ERK)1 by IGF-I. Thus, p53 effects on the IGF axis are more complex than previously appreciated, and overall transform the axis from IGF-mediated mitogenesis to growth inhibition and apoptosis. This has significant implications for how growth hormone and IGF-I can induce growth without also inducing cancer."xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.org/dc/terms/identifier | "doi:10.4161/cbt.5.10.3455"xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/author | "El-Deiry W.S."xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/author | "Shi Z."xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/author | "Wang W."xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/author | "Coleman C.M."xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/author | "MacLachlan T.K."xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/author | "Burns T.F."xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/author | "Grimberg A."xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/name | "Cancer Biol Ther"xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/pages | "1408-1414"xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/title | "Insulin-like growth factor factor binding protein-2 is a novel mediator of p53 inhibition of insulin-like growth factor signaling."xsd:string |
http://purl.uniprot.org/citations/17102589 | http://purl.uniprot.org/core/volume | "5"xsd:string |
http://purl.uniprot.org/citations/17102589 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17102589 |
http://purl.uniprot.org/citations/17102589 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17102589 |
http://purl.uniprot.org/uniprot/#_A0A087WXZ1-mappedCitation-17102589 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17102589 |
http://purl.uniprot.org/uniprot/#_A0A087X1Q1-mappedCitation-17102589 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17102589 |
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http://purl.uniprot.org/uniprot/#_A0A087WT22-mappedCitation-17102589 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17102589 |
http://purl.uniprot.org/uniprot/#_A0A0A0U7X4-mappedCitation-17102589 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17102589 |
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