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p21WAF/CIP1/SDI1 is upregulated due to increased mRNA stability during hydroxyurea-induced senescence of human fibroblasts
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Hyun-Seok | - |
dc.contributor.author | Yeo, Eui-ju | - |
dc.contributor.author | Park, Seong-Hoon | - |
dc.contributor.author | Park, Joo-In | - |
dc.contributor.author | Park, Sang-Chul | - |
dc.contributor.author | Shin, Jong-Yeon | - |
dc.contributor.author | Kim, Min-Ju | - |
dc.contributor.author | Oh, Soo-Jin | - |
dc.contributor.author | Won, Moo-Ho | - |
dc.contributor.author | Kang, Tae-Chun | - |
dc.contributor.author | Park, Jae-Bong | - |
dc.contributor.author | Kim, Jaebong | - |
dc.contributor.author | Kim, Jong-Il | - |
dc.contributor.author | Lee, Hyun-Yong | - |
dc.contributor.author | Lee, Jae-Yong | - |
dc.date.accessioned | 2010-01-06T05:00:04Z | - |
dc.date.available | 2010-01-06T05:00:04Z | - |
dc.date.issued | 2005-08-23 | - |
dc.identifier.citation | Mech Ageing Dev. 2005 Dec;126(12):1255-61. Epub 2005 Aug 18. | en |
dc.identifier.issn | 0047-6374 (Print) | - |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16111738 | - |
dc.identifier.uri | https://hdl.handle.net/10371/26283 | - |
dc.description.abstract | 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. | en |
dc.language.iso | en | en |
dc.publisher | Elsevier | en |
dc.subject | Blotting, Northern | en |
dc.subject | Blotting, Western | en |
dc.subject | Cell Aging | en |
dc.subject | Cells, Cultured | en |
dc.subject | Cyclin-Dependent Kinase Inhibitor p21/*biosynthesis | en |
dc.subject | Dose-Response Relationship, Drug | en |
dc.subject | Fibroblasts/*cytology/metabolism | en |
dc.subject | Genes, Reporter | en |
dc.subject | Humans | en |
dc.subject | Hydroxyurea/metabolism/*pharmacology | en |
dc.subject | Luciferases/metabolism | en |
dc.subject | Nucleic Acid Conformation | en |
dc.subject | Plasmids/metabolism | en |
dc.subject | Promoter Regions, Genetic | en |
dc.subject | RNA, Messenger/*metabolism | en |
dc.subject | Time Factors | en |
dc.subject | Transcription, Genetic | en |
dc.subject | Transfection | en |
dc.subject | Gene Expression Regulation | - |
dc.subject | Up-Regulation | - |
dc.title | p21WAF/CIP1/SDI1 is upregulated due to increased mRNA stability during hydroxyurea-induced senescence of human fibroblasts | en |
dc.type | Article | en |
dc.contributor.AlternativeAuthor | 김현석 | - |
dc.contributor.AlternativeAuthor | 여의주 | - |
dc.contributor.AlternativeAuthor | 박성훈 | - |
dc.contributor.AlternativeAuthor | 박주인 | - |
dc.contributor.AlternativeAuthor | 박상철 | - |
dc.contributor.AlternativeAuthor | 신정연 | - |
dc.contributor.AlternativeAuthor | 김민주 | - |
dc.contributor.AlternativeAuthor | 오수진 | - |
dc.contributor.AlternativeAuthor | 원무호 | - |
dc.contributor.AlternativeAuthor | 강태천 | - |
dc.contributor.AlternativeAuthor | 박재봉 | - |
dc.contributor.AlternativeAuthor | 김재봉 | - |
dc.contributor.AlternativeAuthor | 김종일 | - |
dc.contributor.AlternativeAuthor | 이현용 | - |
dc.contributor.AlternativeAuthor | 이재용 | - |
dc.identifier.doi | 10.1016/j.mad.2005.07.002 | - |
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