Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-3-29
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0021-9541
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
183
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Regulation of the cdk inhibitor p27 and its deregulation in cancer.
pubmed:affiliation
Department of Medicine, University of Toronto, Toronto Ontario, Canada.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't