| Rapamycin decelerates cellular senescence. | |
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MedLine Citation:
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PMID: 19471117 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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When the cell cycle is arrested but cellular growth is not, then cells senesce, permanently losing proliferative potential. Here we demonstrated that the duration of cell cycle arrest determines a progressive loss of proliferative capacity. In human and rodent cell lines, rapamycin (an inhibitor of mTOR) dramatically decelerated loss of proliferative potential caused by ectopic p21, p16 and sodium butyrate-induced p21. Thus, when the cell cycle was arrested by these factors in the presence of rapamycin, cells retained the capacity to resume proliferation, once p21, p16 or sodium butyrate were removed. While rapamycin prevented the permanent loss of proliferative potential in arrested cells, it did not force the arrested cells into proliferation. During cell cycle arrest, rapamycin transformed the irreversible arrest into a reversible condition. Our data demonstrate that senescence can be pharmacologically suppressed. |
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Authors:
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Zoya N Demidenko; Svetlana G Zubova; Elena I Bukreeva; Valery A Pospelov; Tatiana V Pospelova; Mikhail V Blagosklonny |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-06-01 |
Journal Detail:
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Title: Cell cycle (Georgetown, Tex.) Volume: 8 ISSN: 1551-4005 ISO Abbreviation: Cell Cycle Publication Date: 2009 Jun |
Date Detail:
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Created Date: 2009-06-01 Completed Date: 2009-08-14 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 101137841 Medline TA: Cell Cycle Country: United States |
Other Details:
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Languages: eng Pagination: 1888-95 Citation Subset: IM |
Affiliation:
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Oncotarget, Albany, NY, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Butyrates / pharmacology Cell Aging / drug effects*, physiology Cell Cycle / drug effects*, physiology Cell Line Cell Line, Tumor Cyclin-Dependent Kinase Inhibitor p21 / metabolism Humans Isopropyl Thiogalactoside / pharmacology Mice Neoplasm Proteins / metabolism Protein Kinases / drug effects*, metabolism Sirolimus / pharmacology* |
| Grant Support | |
ID/Acronym/Agency:
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1 R41 EY018520-01/EY/NEI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Butyrates; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Neoplasm Proteins; 0/P16 protein, human; 367-93-1/Isopropyl Thiogalactoside; 53123-88-9/Sirolimus; EC 2.7.-/Protein Kinases; EC 2.7.1.-/mTOR protein |
| Comments/Corrections | |
Comment In:
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Cell Cycle. 2009 Jun 15;8(12):1820-1
[PMID:
19471126
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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