Document Detail


Cell cycle control by p53 in normal (3T3) and chemically transformed (Meth A) mouse cells. I. Regulation of p53 expression.
MedLine Citation:
PMID:  2267135     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In addition to controlling the transition of resting normal cells from the G0-state of the cell cycle into S-phase, expression of the cellular protein p53 also seems to be necessary for the proliferation of cycling normal cells in an as yet undefined manner. To further elaborate the role of p53 in growing cells, we analysed p53 expression and its regulation in cells going into, and after release from, growth arrest at the restriction point (R-point) in the G1-phase of the cell cycle, induced by isoleucine depletion. Since growth arrest at the R-point is subject to internal control mechanisms of the cell cycle, this approach allowed us to include in our analyses normal Balb/c 3T3 fibroblasts, as well as cells of the chemically induced Balb/c fibrosarcoma cell line Meth A, expressing mutated p53. Isoleucine depletion induced a viable growth arrest at the R-point in cells of both cell lines, marked by a synchronous shut-down of DNA synthesis when the cells went into growth arrest, and a synchronous resumption of DNA synthesis after a lag period of about 2-4 h when the cells were released from growth arrest, as well as a shift to a G1 DNA content at the R-point. p53 expression in both cell lines showed a phenotypically similar regulation, as its synthesis was specifically reduced at the R-point. At the molecular level, however, p53 expression in growth arrested 3T3 cells was controlled at the transcriptional/post-transcriptional level, whereas control in growth arrested Meth A cells seemed to be at the level of mRNA translation. After release from growth arrest, p53 synthesis in both types of cells was rapidly restored, preceding resumption of total protein synthesis, and exhibiting a p53-specific profile.
Authors:
K Steinmeyer; H Maacke; W Deppert
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Oncogene     Volume:  5     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  1990 Nov 
Date Detail:
Created Date:  1991-02-14     Completed Date:  1991-02-14     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1691-9     Citation Subset:  IM    
Affiliation:
Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Universität Hamburg, Federal Republic of Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Cycle / physiology*
Cell Division
Cell Line
Cell Line, Transformed
DNA / biosynthesis
Fibroblasts / cytology,  metabolism
Fibrosarcoma / chemically induced,  metabolism,  pathology
G1 Phase
Gene Expression Regulation*
Isoleucine / physiology
Kinetics
Methylcholanthrene
Mice
Mice, Inbred BALB C
Mutation
Tumor Suppressor Protein p53 / genetics*,  physiology
Chemical
Reg. No./Substance:
0/Tumor Suppressor Protein p53; 56-49-5/Methylcholanthrene; 73-32-5/Isoleucine; 9007-49-2/DNA

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


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