| Control of the reversibility of cellular quiescence by the transcriptional repressor HES1. | |
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MedLine Citation:
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PMID: 18719287 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The mechanisms by which quiescent cells, including adult stem cells, preserve their ability to resume proliferation after weeks or even years of cell cycle arrest are not known. We report that reversibility is not a passive property of nondividing cells, because enforced cell cycle arrest for a period as brief as 4 days initiates spontaneous, premature, and irreversible senescence. Increased expression of the gene encoding the basic helix-loop-helix protein HES1 was required for quiescence to be reversible, because HES1 prevented both premature senescence and inappropriate differentiation in quiescent fibroblasts. In some human tumors, the HES1 pathway was activated, which allowed these cells to evade differentiation and irreversible cell cycle arrest. We conclude that HES1 safeguards against irreversible cell cycle exit both during normal cellular quiescence and pathologically in the setting of tumorigenesis. |
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Authors:
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Liyun Sang; Hilary A Coller; James M Roberts |
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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 |
Journal Detail:
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Title: Science (New York, N.Y.) Volume: 321 ISSN: 1095-9203 ISO Abbreviation: Science Publication Date: 2008 Aug |
Date Detail:
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Created Date: 2008-08-22 Completed Date: 2008-09-03 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 0404511 Medline TA: Science Country: United States |
Other Details:
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Languages: eng Pagination: 1095-100 Citation Subset: IM |
Affiliation:
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Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Basic Helix-Loop-Helix Transcription Factors
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genetics,
metabolism* Cell Aging Cell Cycle* Cell Differentiation Cell Line Cell Line, Tumor Cell Proliferation* Cyclin-Dependent Kinase Inhibitor p21 / metabolism Fibroblasts / cytology*, metabolism Homeodomain Proteins / genetics, metabolism* Humans Muscle Development MyoD Protein / metabolism Receptors, Notch / metabolism Recombinant Fusion Proteins / metabolism Repressor Proteins / genetics, metabolism* Rhabdomyosarcoma / metabolism, pathology Signal Transduction Transduction, Genetic |
| Grant Support | |
ID/Acronym/Agency:
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P50 GM071508/GM/NIGMS NIH HHS; P50 GM071508-05/GM/NIGMS NIH HHS; R01 CA118043-03/CA/NCI NIH HHS; //Howard Hughes Medical Institute |
| Chemical | |
Reg. No./Substance:
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0/Basic Helix-Loop-Helix Transcription Factors; 0/Cdkn1a protein, mouse; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Homeodomain Proteins; 0/MyoD Protein; 0/MyoD1 myogenic differentiation protein; 0/Receptors, Notch; 0/Recombinant Fusion Proteins; 0/Repressor Proteins; 0/TLE1 protein, human; 149348-15-2/HES1 protein, human |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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