| pubmed-article:9491783 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0083867 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0205950 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0521457 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0123259 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0021666 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:9491783 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:9491783 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:9491783 | pubmed:dateCreated | 1998-3-12 | lld:pubmed |
| pubmed-article:9491783 | pubmed:abstractText | Osteogenic protein-1 (OP-1 or BMP-7) stimulates new bone formation in vivo and induces cell proliferation and differentiation of osteoblasts in vitro. Previous studies from our laboratory revealed that OP-1 led to a two- to threefold increase in steady-state insulin-like growth factor-I (IGF-I) and IGF-II mRNA levels and a fivefold decrease in IGF-binding protein-5 (IGFBP-5) mRNA levels in primary cultures of fetal rat calvaria (FRC) cells. In the present study, we determined whether the effects of OP-1 were at the transcriptional or posttranscriptional level. OP-1 increased the half-life of the IGF-I mRNA from 6 to 17 h without changing the level of IGF-I nuclear pre-mRNA. In transiently transfected FRC cells, the luciferase activity driven by the -1122/+362 or the -133/+362 IGF-I exon 1 promoter fragment was not changed by OP-1. Similar results were observed using the -1500/+44 or -362/+44 IGF-I exon 2 promoter constructs. Effects of OP-1 on IGF-I mRNA were independent of cell division, as they remained elevated in the presence of hydroxyurea. Cycloheximide inhibited moderately the OP-1-induced increase in IGF-I mRNA, suggesting partial dependency on protein synthesis. On the other hand, the IGF-II nuclear pre-mRNA levels were increased by OP-1 but the half-life of the mature IGF-II mRNA was not affected. Effects of OP-1 on IGF-II mRNA were also independent of cell division, but were dependent on protein synthesis. OP-1 caused a 43-50% reduction in the level of IGFBP-5 nuclear pre-mRNA transcripts and a 40% decrease in the IGFBP-5 promoter activity in FRC cells transfected with the -1278/+1 IGFBP-5 promoter fragment. The half-life of the mature IGFBP-5 mRNA was not affected by OP-1. Hydroxyurea did not prevent the OP-1-induced reduction in IGFBP-5 mRNA. The level of IGFBP-5 mRNA was barely detectable in the presence of cycloheximide, and further suppressive effect of OP-1 on IGFBP-5 mRNA could not be determined. In conclusion, OP-1 regulates IGF-I gene expression at the posttranscriptional level, but regulates IGF-II and IGFBP-5 gene expression at the transcriptional level. | lld:pubmed |
| pubmed-article:9491783 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9491783 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9491783 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9491783 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9491783 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9491783 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:9491783 | pubmed:issn | 0021-9541 | lld:pubmed |
| pubmed-article:9491783 | pubmed:author | pubmed-author:LeeJ CJC | lld:pubmed |
| pubmed-article:9491783 | pubmed:author | pubmed-author:LeeY FYF | lld:pubmed |
| pubmed-article:9491783 | pubmed:author | pubmed-author:AdamsM PMP | lld:pubmed |
| pubmed-article:9491783 | pubmed:author | pubmed-author:DuanCC | lld:pubmed |
| pubmed-article:9491783 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9491783 | pubmed:volume | 175 | lld:pubmed |
| pubmed-article:9491783 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9491783 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9491783 | pubmed:pagination | 78-88 | lld:pubmed |
| pubmed-article:9491783 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:9491783 | pubmed:meshHeading | pubmed-meshheading:9491783-... | lld:pubmed |
| pubmed-article:9491783 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9491783 | pubmed:articleTitle | Osteogenic protein-1 regulates insulin-like growth factor-I (IGF-I), IGF-II, and IGF-binding protein-5 (IGFBP-5) gene expression in fetal rat calvaria cells by different mechanisms. | lld:pubmed |
| pubmed-article:9491783 | pubmed:affiliation | Department of Biochemistry, The University of Texas Health Science Center, San Antonio 78284-7760, USA. | lld:pubmed |
| pubmed-article:9491783 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9491783 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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