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Changes in Cobalamin Metabolism Are Associated with the Altered Methionine Auxotrophy of Highly Growth Autonomous Human Melanoma Cells by Robert G. Liteplo; Sheridan E. Hipwell; David S. Rosenblatt; Sue Sillaots; Helena Lue‐Shing is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

## Abstract Our aim was to identify the biochemical defect responsible for the inability of highly growth autonomous human tumor cells to proliferate in culture medium devoid of methionine, but containing homocysteine and 5‐methyltetrahydrofolic acid. We have adopted the terms “homocysteine‐responsive” and “homocysteine‐nonresponsive” to describe cells which can or cannot proliferate in methionine‐free homocysteine‐supplemented medium. Using a panel of genetically related homocysteine‐responsive and ‐nonresponsive human melanoma cell lines, the results from a number of experiments indicate that acquisition of the “homocysteine‐nonresponsive phenotype” is associated with the reduced intracellular accumulation of methyl‐cobalamin, a critical cofactor of the methionine synthase enzyme. When in vitro methionine synthase assays were performed in the presence of exogenously added methyl‐cobalamin, specific methionine synthase activity in extracts obtained from homocysteine‐responsive cells was only twofold greater than that observed with extracts prepared from homocysteine‐nonresponsive cells. However, when exogenous methyl‐cobalamin was omitted from the enzyme assays, methionine synthas

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Author
Robert G. Liteplo; Sheridan E. Hipwell; David S. Rosenblatt; Sue Sillaots; Helena Lue‐Shing
Publisher
John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0021-9541)
Published
1991
Language
EN
Field
Biochemistry, Genetics and Molecular Biology (Life Sciences)