pubmed-article:19033198 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19033198 | lifeskim:mentions | umls-concept:C0086661 | lld:lifeskim |
pubmed-article:19033198 | lifeskim:mentions | umls-concept:C1510411 | lld:lifeskim |
pubmed-article:19033198 | lifeskim:mentions | umls-concept:C0069141 | lld:lifeskim |
pubmed-article:19033198 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:19033198 | pubmed:issue | 48 | lld:pubmed |
pubmed-article:19033198 | pubmed:dateCreated | 2008-12-3 | lld:pubmed |
pubmed-article:19033198 | pubmed:abstractText | The transcription factor c-Myc is essential for cellular proliferation and is one of the most frequently activated oncogenes, but the molecular mechanism mediating its critical role in transformation is unclear. Like c-Myc, multifunctional nucleophosmin (NPM) is tightly regulated during proliferation and is overexpressed in several different types of cancer. Overexpression of NPM enhances proliferation and oncogene-mediated transformation, but the mechanism mediating these effects is unknown. We examined whether NPM stimulates proliferation and transformation by affecting c-Myc. Here, we show that NPM is essential for the activities of oncogenic c-Myc and that overexpressed NPM dramatically stimulates c-Myc-induced hyperproliferation and transformation. Endogenous and exogenous NPM directly interact with c-Myc and regulate the expression of endogenous c-Myc target genes at the promoter. Therefore, NPM is a key cofactor for the transforming activity of c-Myc and the interaction with c-Myc may mediate the enhancement of proliferation and transformation induced by NPM overexppression. | lld:pubmed |
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pubmed-article:19033198 | pubmed:language | eng | lld:pubmed |
pubmed-article:19033198 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19033198 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19033198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19033198 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19033198 | pubmed:month | Dec | lld:pubmed |
pubmed-article:19033198 | pubmed:issn | 1091-6490 | lld:pubmed |
pubmed-article:19033198 | pubmed:author | pubmed-author:BooneDavidD | lld:pubmed |
pubmed-article:19033198 | pubmed:author | pubmed-author:HannStephen... | lld:pubmed |
pubmed-article:19033198 | pubmed:author | pubmed-author:LiZhaoliangZ | lld:pubmed |
pubmed-article:19033198 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19033198 | pubmed:day | 2 | lld:pubmed |
pubmed-article:19033198 | pubmed:volume | 105 | lld:pubmed |
pubmed-article:19033198 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19033198 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19033198 | pubmed:pagination | 18794-9 | lld:pubmed |
pubmed-article:19033198 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:19033198 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:19033198 | pubmed:articleTitle | Nucleophosmin interacts directly with c-Myc and controls c-Myc-induced hyperproliferation and transformation. | lld:pubmed |
pubmed-article:19033198 | pubmed:affiliation | Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232-2175, USA. | lld:pubmed |
pubmed-article:19033198 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19033198 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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