| pubmed-article:10779549 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C0004903 | lld:lifeskim |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C0001721 | lld:lifeskim |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C0021666 | lld:lifeskim |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:10779549 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:10779549 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:10779549 | pubmed:dateCreated | 2000-6-13 | lld:pubmed |
| pubmed-article:10779549 | pubmed:abstractText | In both human and mouse, the Igf2 gene, localized on chromosomes 11 and 7, respectively, is expressed from the paternally inherited chromosome in the majority of tissues. Insulin-like growth factor-II (IGF-II) plays an important role in embryonic growth, and aberrant IGF2 expression has been documented in several human pathologies, such as Beckwith-Wiedemann syndrome (BWS), and a wide variety of tumors. Human and mouse genetic data strongly implicate another gene, CDKN1C (p57(kip2)), located in the same imprinted gene cluster on human chromosome II, in BWS. p57(KIP2) is a cyclin-dependent kinase inhibitor and is required for normal mouse embryonic development. Mutations in CDKN1C (p57(kip2)) have been identified in a small proportion of patients with BWS, and removal of the gene from mice by targeted mutagenesis produces a phenotype with elements in common with this overgrowth syndrome. Patients with BWS with biallelic expression of IGF2 or with a CDKN1C (p57(kip2)) mutation, as well as overlapping phenotypes observed in two types of mutant mice, the p57(kip2) knockout and IGF-II-overexpressing mice, strongly suggest that the genes may act in a common pathway of growth control in situations where Igf2 expression is abnormal. Herein, we show that p57(kip2) expression is reduced on IGF-II treatment of primary embryo fibroblasts in a dose-dependent manner. In addition, p57(kip2) expression is down-regulated in mice with high serum levels of IGF-II. These data suggest that the effects of increased IGF-II in BWS may, in part, be mediated through a decrease in p57(kip2) gene expression. | lld:pubmed |
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| pubmed-article:10779549 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10779549 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10779549 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10779549 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10779549 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10779549 | pubmed:month | May | lld:pubmed |
| pubmed-article:10779549 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:10779549 | pubmed:author | pubmed-author:SmithJJ | lld:pubmed |
| pubmed-article:10779549 | pubmed:author | pubmed-author:SchofieldP... | lld:pubmed |
| pubmed-article:10779549 | pubmed:author | pubmed-author:Ferguson-Smit... | lld:pubmed |
| pubmed-article:10779549 | pubmed:author | pubmed-author:GrandjeanVV | lld:pubmed |
| pubmed-article:10779549 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10779549 | pubmed:day | 9 | lld:pubmed |
| pubmed-article:10779549 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:10779549 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10779549 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10779549 | pubmed:pagination | 5279-84 | lld:pubmed |
| pubmed-article:10779549 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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