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p53 prevents immature escaping from cell cycle G2 checkpoint arrest through inhibiting cdk2-dependent NF-Y phosphorylation.
MedLine Citation:
PMID:  19771247     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
PURPOSE: Recent studies have suggested that p53 regulates the G2 checkpoint in the cell cycle and this function is required for the maintenance of genomic integrity. In this study, we addressed a role of p53 in escaping from cell cycle G2 arrest following DNA damage.
MATERIALS AND METHODS: Cell cycle checkpoint arrest in the human colon cancer cell line HCT116 and its derivatives carry p53 or p21 deletions, were examined by FACS analysis, immunoprecipitation, Western blot and IP-kinase assay.
RESULTS: While the cells with functional p53 were arrested at both the G1 and G2 checkpoints, the p53-deficient cells failed to arrest at G1, but they were arrested at G2. However, the p53-deficient cells failed to sustain G2 checkpoint arrest and they entered mitosis earlier than did the p53-positive cells and so this resulted in extensive cell death. Cdc2 kinase becomes reactivated in p53-deficient cells in association with entry into mitosis, but not in the p53-positive cells. Upon DNA damage, the p21-deficient cells, like the p53-negative cells, not only failed to repress cdk2-dependent NF-Y phosphorylation, but they also failed to repress the expression of such cell cycle G2-regulatory genes as cdc2, cyclin B, RNR-R2 and cdc25C, which have all been previously reported as targets of NF-Y transcription factor.
CONCLUSIONS: p53 is essential to prevent immature escaping from cell cycle G2 checkpoint arrest through p21-mediated cdk2 inactivation, and this leads to inhibition of cdk2-dependent NF-Y phosphorylation and NF-Y dependent transcription of the cell cycle G2-regulatory genes, including cdc2 and cyclin B.
Authors:
Un-Jung Yun; Heui-Dong Park; Deug Y Shin
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Publication Detail:
Type:  Journal Article     Date:  2006-12-31
Journal Detail:
Title:  Cancer research and treatment : official journal of Korean Cancer Association     Volume:  38     ISSN:  1598-2998     ISO Abbreviation:  Cancer Res Treat     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2009-09-22     Completed Date:  2010-06-25     Revised Date:  2013-05-23    
Medline Journal Info:
Nlm Unique ID:  101155137     Medline TA:  Cancer Res Treat     Country:  Korea (South)    
Other Details:
Languages:  eng     Pagination:  224-8     Citation Subset:  -    
Affiliation:
National Research Laboratory of Cell Cycle Regulation, Department of Microbiology, Dankook University College of Medicine, Cheonan, Korea.
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