Document Detail

Analyzing the G2/M checkpoint.
MedLine Citation:
PMID:  15187249     Owner:  NLM     Status:  MEDLINE    
The G2 checkpoint prevents cells from entering mitosis when DNA is damaged, providing an opportunity for repair and stopping the proliferation of damaged cells. Because the G2 checkpoint helps to maintain genomic stability, it is an important focus in understanding the molecular causes of cancer. Many different methods have been used to investigate the G2 checkpoint and uncover some of the underlying mechanisms. Because cell-cycle controls are highly conserved, a remarkable synergy between the genetic power of model organisms and biochemical analyses is possible and has uncovered control mechanisms that operate in many diverse species, including humans. Cdc2, the cyclin-dependent kinase that normally drives cells into mitosis, is an important target of pathways that mediate rapid arrest in G2 in response to DNA damage. Additional pathways ensure that the arrest is stably maintained. When mammalian cells contain damaged DNA, the p53 tumor suppressor and the Rb family of transcriptional repressors work together to downregulate a large number of genes that encode proteins required for G2 and M. Elimination of these essential cell cycle proteins helps to keep the cells arrested in G2.
George R Stark; William R Taylor
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Methods in molecular biology (Clifton, N.J.)     Volume:  280     ISSN:  1064-3745     ISO Abbreviation:  Methods Mol. Biol.     Publication Date:  2004  
Date Detail:
Created Date:  2004-06-09     Completed Date:  2004-09-09     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9214969     Medline TA:  Methods Mol Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  51-82     Citation Subset:  IM    
Department of Molecular Biology, Lerner Research Institute, The Cleveland Clinic Foundation, Ohio, USA.
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MeSH Terms
CDC2 Protein Kinase / metabolism
Cell Cycle
Chromatin / metabolism
DNA Damage
G2 Phase*
Microscopy / instrumentation
Models, Biological
Retinoblastoma Protein / metabolism
Time Factors
Tumor Suppressor Protein p53 / metabolism
Grant Support
Reg. No./Substance:
0/Chromatin; 0/Retinoblastoma Protein; 0/Tumor Suppressor Protein p53; EC Protein Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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