Document Detail


Methionine metabolism defect in cells transfected with an activated HRAS1 oncogene.
MedLine Citation:
PMID:  3817009     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Methionine dependence is a metabolic defect characterized by the inability of eukaryotic cells in culture to proliferate in a medium where methionine has been replaced by its immediate metabolic precursor, homocysteine. This defect has been reported to be a specific property of diverse tumour-derived and transformed cell lines; normal cell strains grow well under the above culture conditions. The basis of methionine requirement in such cells is not known. We asked whether this defect might be controlled by activated oncogenes and in particular by the mutated (activated) HRAS1 oncogene derived from the EJ/T24 human carcinoma line. We report that this oncogene induces methionine requirement after transfection in non-transformed immortalized rat cells.
Authors:
L Vanhamme; C Szpirer
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Experimental cell research     Volume:  169     ISSN:  0014-4827     ISO Abbreviation:  Exp. Cell Res.     Publication Date:  1987 Mar 
Date Detail:
Created Date:  1987-04-08     Completed Date:  1987-04-08     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0373226     Medline TA:  Exp Cell Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  120-6     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Division
Cell Line
Cell Transformation, Neoplastic*
Clone Cells
Humans
Liver
Methionine / metabolism*
Nucleic Acid Hybridization
Oncogenes*
Plasmids
Rats
Transcription, Genetic
Transformation, Genetic
Chemical
Reg. No./Substance:
63-68-3/Methionine

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


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