Document Detail

Transcriptional targets of p53 that regulate cellular proliferation.
MedLine Citation:
PMID:  17361486     Owner:  NLM     Status:  MEDLINE    
In response to various forms of cellular stress, including DNA damage, ribonucleotide depletion, and abnormal proliferative signals, p53 becomes activated as a transcription factor, targeted genes that induce cell-cycle arrest and apoptosis. Eliminating damaged, stressed, or abnormally proliferating cells from the replicating cell population prevents the propagation of potentially cancer-prone cells. Here we focus on the transcriptional targets of p53 that regulate the cell cycle. p53 Induction of G1/ S cell-cycle arrest is largely attributed to the transcriptional upregulation of p21WAF1, and more recently, to the transcriptional repression of c-MYC. The role of p53 in G2/M cell-cycle arrest in response to DNA damage is more complex, involving multiple targets that can generally be considered to impinge upon either the cell cycle (e.g., Cyclin-B, cdc2, cdc25C) or the mitotic machinery (i.e., Topoisomerase II, B99/Gtse-1, and MAP4). The ability of p53 to regulate these two type of gene targets may reflect p53-mediated early versus late events in the G2/M cell-cycle arrest response. Together the information presented illustrates the need for further studies to precisely delineate the nature of G2/M cell-cycle arrest in response to cell stress, and defines the role of p53 in what is likely an important mechanism of tumor suppression.
Lauren Brown; Sarah Boswell; Lakshmi Raj; Sam W Lee
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Critical reviews in eukaryotic gene expression     Volume:  17     ISSN:  1045-4403     ISO Abbreviation:  Crit. Rev. Eukaryot. Gene Expr.     Publication Date:  2007  
Date Detail:
Created Date:  2007-03-15     Completed Date:  2007-04-17     Revised Date:  2007-07-11    
Medline Journal Info:
Nlm Unique ID:  9007261     Medline TA:  Crit Rev Eukaryot Gene Expr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  73-85     Citation Subset:  IM    
Cutaneous Biology Research Center, Massachussetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
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MeSH Terms
Cell Cycle / genetics*
Cell Cycle Proteins / genetics*
Cell Proliferation
Transcription, Genetic*
Tumor Suppressor Protein p53 / metabolism*
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Tumor Suppressor Protein p53

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