Document Detail


Control of the reversibility of cellular quiescence by the transcriptional repressor HES1.
MedLine Citation:
PMID:  18719287     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Liyun Sang; Hilary A Coller; James M Roberts
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Science (New York, N.Y.)     Volume:  321     ISSN:  1095-9203     ISO Abbreviation:  Science     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-08-22     Completed Date:  2008-09-03     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  0404511     Medline TA:  Science     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1095-100     Citation Subset:  IM    
Affiliation:
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
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MeSH Terms
Descriptor/Qualifier:
Basic Helix-Loop-Helix Transcription Factors / 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:
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:
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

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