http://purl.uniprot.org/citations/18212051 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/18212051 | http://www.w3.org/2000/01/rdf-schema#comment | "Steroid receptor coactivator 3 (SRC-3/AIB1/ACTR/NCoA-3) is a transcriptional coactivator for nuclear receptors including vitamin D receptor (VDR). Growth hormone (GH) regulates insulin-like growth factor I (IGF-I) expression, and IGF-I forms complexes with acid-labile subunit (ALS) and IGF-binding protein 3 (IGFBP-3) to maintain its circulating concentration and endocrine function. This study demonstrated that the circulating IGF-I was significantly reduced in SRC-3(-/-) mice with the C57BL/6J background. However, SRC-3 deficiency affected neither GH nor ALS expression. The low IGF-I level in SRC-3(-/-) mice was not due to the failure of IGF-I mRNA and protein synthesis but was a consequence of rapid degradation. The rapid IGF-I degradation was associated with drastically reduced IGFBP-3 levels. Because IGF-I and IGFBP-3 stabilize each other, SRC-3(-/-) mice were crossbred with the liver-specific transthyretin (TTR)-IGF-I transgenic mice to assess the relationship between reduced IGF-I and IGFBP-3. In SRC-3(-/-)/TTR-IGF-I mice, the IGF-I level was significantly increased over that in SRC-3(-/-) mice, but the IGFBP-3 level failed to increase proportionally, indicating that the low IGFBP-3 level is a responsible factor that limits the IGF-I level in SRC-3(-/-) mice. Furthermore, IGFBP-3 mRNA was reduced in SRC-3(-/-) mice. The IGFBP-3 promoter activity induced by vitamin D, through VDR, was diminished in SRC-3(-/-) cells, suggesting an important role of SRC-3 in VDR-mediated transactivation of the IGFBP-3 gene. In agreement with the role of SRC-3 in VDR function, the expression of several VDR target genes was also reduced in SRC-3(-/-) mice. Therefore, SRC-3 maintains IGF-I in the circulation through enhancing VDR-regulated IGFBP-3 expression."xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.01163-07"xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/author | "Chen X."xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/author | "Wang S."xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/author | "Xu J."xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/author | "Liao L."xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/author | "Parlow A.F."xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/name | "Mol Cell Biol"xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/pages | "2460-2469"xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/title | "Steroid receptor coactivator 3 maintains circulating insulin-like growth factor I (IGF-I) by controlling IGF-binding protein 3 expression."xsd:string |
http://purl.uniprot.org/citations/18212051 | http://purl.uniprot.org/core/volume | "28"xsd:string |
http://purl.uniprot.org/citations/18212051 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18212051 |
http://purl.uniprot.org/citations/18212051 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/18212051 |
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