期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 278, 期 8, 页码 5952-5955出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M212194200
关键词
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Mild hyperhomocysteinemia is an independent risk factor for cardiovascular disease. Homocysteine, a nonprotein amino acid, is formed from S-adenosylhomocysteine and partially secreted into plasma. A potential source for homocysteine is methylation of the lipid phosphatidylethanolamine to phosphatidylcholine by phosphatidylethanolamine N-methyltransferase in the liver. We show that mice that lack phosphatidylethanolamine N-methyltransferase have plasma levels of homocysteine that are similar to50% of those in wild-type mice. Hepatocytes isolated from methyltransferase-deficient mice secrete similar to50% less homocysteine. Rat hepatoma cells transfected with phosphatidylethanolamine N-methyltransferase secrete more homocysteine than wild-type cells. Thus, phosphatidylethanolamine N-methyltransferase is an important source of plasma homocysteine and a potential therapeutic target for hyperhomocysteinemia.
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