Hirsh J, Berg P
Proc Natl Acad Sci U S A. 1976 May;73(5):1518-22. doi: 10.1073/pnas.73.5.1518.
Unlike normal cells, malignant rat and two simian virus 40-transformed human cell lines can neither grow nor survive in B12- and folate-supplemented media in which methionine is replaced by homocysteine. Yet three lines of evidence indicate that the malignant and transformed cells synthesize large amounts of methionine endogenously through the reaction catalyzed by 5-methyltetrahydropterolyl-L-glutamate: L-homocysteine S-methyltransferase (EC 2.1.1.13). (1) The activities of this methyltransferase were comparable in extracts of malignant and normal cells. (2) The uptake of radioactive label from [5-14C]methyltetrahydropteroyl-L-glutamic acid (5-Me-H4PteGlu) was at least as great in the malignant cells as in the normals and was nearly totally dependent on the addition of homocysteine, the methyl acceptor; furthermore, 59-84% of the label incorporated by cells was recovered as methionine.
与正常细胞不同，恶性大鼠细胞和两种猿猴病毒40转化的人类细胞系在以同型半胱氨酸替代甲硫氨酸的、添加了维生素B12和叶酸的培养基中既无法生长也无法存活。然而，有三条证据表明，恶性细胞和转化细胞通过由5-甲基四氢蝶酰-L-谷氨酸：L-同型半胱氨酸S-甲基转移酶（EC 2.1.1.13）催化的反应内源性地合成大量甲硫氨酸。（1）这种甲基转移酶在恶性细胞和正常细胞提取物中的活性相当。（2）恶性细胞从[5-14C]甲基四氢蝶酰-L-谷氨酸（5-Me-H4PteGlu）摄取放射性标记物的能力至少与正常细胞一样强，并且几乎完全依赖于添加作为甲基受体的同型半胱氨酸；此外，细胞摄取的标记物中有59%-84%以甲硫氨酸的形式回收。
