pubmed-article:16111738 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16111738 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:16111738 | lifeskim:mentions | umls-concept:C0231337 | lld:lifeskim |
pubmed-article:16111738 | lifeskim:mentions | umls-concept:C1705522 | lld:lifeskim |
pubmed-article:16111738 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
pubmed-article:16111738 | lifeskim:mentions | umls-concept:C0678226 | lld:lifeskim |
pubmed-article:16111738 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
pubmed-article:16111738 | lifeskim:mentions | umls-concept:C0249197 | lld:lifeskim |
pubmed-article:16111738 | lifeskim:mentions | umls-concept:C1257757 | lld:lifeskim |
pubmed-article:16111738 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:16111738 | pubmed:dateCreated | 2005-11-15 | lld:pubmed |
pubmed-article:16111738 | pubmed:abstractText | Hydoxyurea induces senescence-like growth arrest in normal human fibroblasts. p21(WAF/CIP1/SDI1), a cyclin dependent kinase inhibitor, was found to be upregulated during this growth arrest. Levels of p21(WAF/CIP1/SDI1) protein and mRNA were increased nine-fold by hydroxyurea in these cells. In order to determine whether p21(WAF/CIP1/SDI1) mRNA is increased by hydroxyurea at the transcriptional level, human fibroblast cells were transfected with reporter constructs containing a p21(WAF/CIP1/SDI1) promoter fragment and then treated with hydroxyurea. The luciferase activities in the reporter-transfected fibroblast cells were not increased by hydroxyurea, indicating that p21(WAF/CIP1/SDI1) transcription was not elevated by hydroxyurea. The half-life of the p21(WAF/CIP1/SDI1) mRNA was increased by 2.5-fold but that of p21(WAF/CIP1/SDI1) protein was not. Our results suggest that increased mRNA stability is the major mechanism of p21(WAF/CIP1/SDI1) elevation in the hydroxyurea-induced growth arrest of human fibroblasts. | lld:pubmed |
pubmed-article:16111738 | pubmed:language | eng | lld:pubmed |
pubmed-article:16111738 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16111738 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16111738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16111738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16111738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16111738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16111738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16111738 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16111738 | pubmed:month | Dec | lld:pubmed |
pubmed-article:16111738 | pubmed:issn | 0047-6374 | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:KimJong-IlJI | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:ParkJae-BongJ... | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:LeeJae-YongJY | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:KimJaebongJ | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:ParkSang-Chul... | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:WonMoo-HoMH | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:KimMin-JuMJ | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:ParkSeong-Hoo... | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:ParkJoo-InJI | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:OhSoo-JinSJ | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:KimHyun-SeokH... | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:YeoEui-juEJ | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:ShinJong-Yeon... | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:KangTae-ChunT... | lld:pubmed |
pubmed-article:16111738 | pubmed:author | pubmed-author:LeeHyun-YongH... | lld:pubmed |
pubmed-article:16111738 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16111738 | pubmed:volume | 126 | lld:pubmed |
pubmed-article:16111738 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16111738 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16111738 | pubmed:pagination | 1255-61 | lld:pubmed |
pubmed-article:16111738 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:16111738 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:16111738 | pubmed:articleTitle | p21WAF/CIP1/SDI1 is upregulated due to increased mRNA stability during hydroxyurea-induced senescence of human fibroblasts. | lld:pubmed |
pubmed-article:16111738 | pubmed:affiliation | Department of Biochemistry, College of Medicine, Hallym University, 1 Okchon-dong, Chuncheon, Gangwon-do 200-702, South Korea. | lld:pubmed |
pubmed-article:16111738 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16111738 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:1026 | entrezgene:pubmed | pubmed-article:16111738 | lld:entrezgene |
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