| Estrogen prevents senescence through induction of WRN, Werner syndrome protein. | |
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MedLine Citation:
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PMID: 20395656 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Werner syndrome is a well-known human progeria. It has been revealed that loss of human WRN is a causal factor of this disease. Since pathological features of Werner syndrome resemble those of menopausal women and become apparent during puberty, we examined the effect of estrogen on WRN gene expression. Here, we reveal that WRN is induced by estrogen but not testosterone. Treatment with estrogen can induce WRN expression at the transcription and translation level in a human breast cell line. Forced expression of the estrogen receptor can restore the responsiveness of WRN to estrogen in a non-responsive cell line. Treatment with estrogen can block DNA damage-induced senescence. Moreover, WRN is suppressed by ATR that is activated by DNA damage, whereas WRN can be induced by ATR elimination. Our results suggest that WRN is essential for prevention of senescence. In addition, our results imply that the reduction of WRN in menopause could be an important factor for menopausal syndrome. |
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Authors:
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Su-Jin Lee; Sun-Hye Lee; Nam-Chul Ha; Bum-Joon Park |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-04-15 |
Journal Detail:
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Title: Hormone research in pædiatrics Volume: 74 ISSN: 1663-2826 ISO Abbreviation: Horm Res Paediatr Publication Date: 2010 |
Date Detail:
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Created Date: 2010-07-19 Completed Date: 2010-11-15 Revised Date: 2011-03-22 |
Medline Journal Info:
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Nlm Unique ID: 101525157 Medline TA: Horm Res Paediatr Country: Switzerland |
Other Details:
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Languages: eng Pagination: 33-40 Citation Subset: IM |
Copyright Information:
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Copyright 2010 S. Karger AG, Basel. |
Affiliation:
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Department of Molecular Biology, College of Natural Science, Pusan National University, Busan, Republic of Korea. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Blotting, Western Cell Aging / drug effects*, genetics, physiology Cell Cycle Proteins / metabolism Cell Line, Tumor Child DNA Damage Estrogen Receptor alpha / genetics, metabolism* Estrogens / pharmacology* Exodeoxyribonucleases / biosynthesis*, genetics Female Gene Expression Regulation / drug effects HCT116 Cells Humans Immunohistochemistry Protein-Serine-Threonine Kinases / metabolism RNA, Messenger / biosynthesis, genetics RecQ Helicases / biosynthesis*, genetics Reverse Transcriptase Polymerase Chain Reaction Testosterone / pharmacology Transcription, Genetic / drug effects Werner Syndrome / drug therapy, genetics, metabolism*, pathology* |
| Chemical | |
Reg. No./Substance:
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0/Cell Cycle Proteins; 0/Estrogen Receptor alpha; 0/Estrogens; 0/RNA, Messenger; 58-22-0/Testosterone; EC 2.7.1.-/ATR protein, human; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 3.1.-/Exodeoxyribonucleases; EC 3.6.1.-/RecQ Helicases; EC 3.6.1.-/WRN protein, human |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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