Linked Life Data

12800980

Source:http://linkedlifedata.com/resource/pubmed/id/12800980

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-6-12
pubmed:abstractText
Involvement of CDK2 in glucocorticoid-mediated S-phase lengthening was analyzed in this work. Dexamethasone (DXM) treatment of PHA-stimulated lymphocytes induced a decrease in CDK2 mRNA expression without any change in mRNA stability. This glucocorticoid-induced decrease in CDK2 mRNA expression could be suppressed by cycloheximide treatment. These results support the hypothesis of an indirect effect of DXM at the transcriptional level. Furthermore, CDK2 protein expression also decreased while the rate of protein synthesis and stability remained unchanged, suggesting a second post-translational level of regulation with the preferential degradation of a CDK2 protein stock fraction. The analysis of co-precipitated proteins showed that glucocorticoids induced modifications of protein complex composition. We found i) a preservation of the linkage capability of CDK2 for cyclin E and A, ii) a relative increase in p27kip1 linkage, and iii) a decrease in p21waf1 complexed with CDK2. As a consequence of CDK2 decrease and modifications of protein complex composition, pRb and histone H1 kinase activity of CDK2 was profoundly decreased. All these results pinpoint the role of CDK2 in glucocorticoid-induced S-phase lengthening and the potential activator role of p21waf1 for CDK2 in human lymphocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0171-9335
pubmed:author
pubmed:issnType
Print
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
253-61
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
CDK2 is involved in the S-phase lengthening induced by glucocorticoids in normal human lymphocytes.
pubmed:affiliation
Laboratoire de Cytologie Analytique, Faculté de Médecine, INSERM U.453, Lyon, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't