| pubmed-article:10699961 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10699961 | lifeskim:mentions | umls-concept:C0006826 | lld:lifeskim |
| pubmed-article:10699961 | lifeskim:mentions | umls-concept:C0169665 | lld:lifeskim |
| pubmed-article:10699961 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:10699961 | lifeskim:mentions | umls-concept:C1880287 | lld:lifeskim |
| pubmed-article:10699961 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:10699961 | pubmed:dateCreated | 2000-3-29 | lld:pubmed |
| pubmed-article:10699961 | pubmed:abstractText | p27 is a cell cycle inhibitor whose cellular abundance increases in response to many antimitogenic stimuli. In this review, we summarize the current knowledge on p27 function and its regulation by synthesis and by ubiquitin-mediated degradation. Importantly, p27 degradation is enhanced in many aggressive human tumors. The frequency with which this is observed suggests that loss of p27 may confer a growth advantage to these cancers. From a practical point of view, immunodetection of p27 in tumors may prove to be useful in the assessment of prognosis and may ultimately influence the therapy of this disease. | lld:pubmed |
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| pubmed-article:10699961 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10699961 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10699961 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10699961 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10699961 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10699961 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10699961 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10699961 | pubmed:issn | 0021-9541 | lld:pubmed |
| pubmed-article:10699961 | pubmed:author | pubmed-author:PaganiGG | lld:pubmed |
| pubmed-article:10699961 | pubmed:author | pubmed-author:SlingerlandJJ | lld:pubmed |
| pubmed-article:10699961 | pubmed:copyrightInfo | Copyright 2000 Wiley-Liss, Inc. | lld:pubmed |
| pubmed-article:10699961 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10699961 | pubmed:volume | 183 | lld:pubmed |
| pubmed-article:10699961 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10699961 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10699961 | pubmed:pagination | 10-7 | lld:pubmed |
| pubmed-article:10699961 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:10699961 | pubmed:meshHeading | pubmed-meshheading:10699961... | lld:pubmed |
| pubmed-article:10699961 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10699961 | pubmed:articleTitle | Regulation of the cdk inhibitor p27 and its deregulation in cancer. | lld:pubmed |
| pubmed-article:10699961 | pubmed:affiliation | Department of Medicine, University of Toronto, Toronto Ontario, Canada. | lld:pubmed |
| pubmed-article:10699961 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10699961 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10699961 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:10699961 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:10699961 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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