Law R E, Ferro A J
J Bacteriol. 1980 Jul;143(1):427-31. doi: 10.1128/jb.143.1.427-431.1980.
S-Adenoxyl-L-methionine (SAM) inhibited leucine transport in Saccharomyces cerevisiae. By using a mutant defective in the active transport of SAM, we demonstrated that the inhibitory effect was exerted at an extracellular site. Cells preincubated wtih SAM for 120 min became refractory to its inhibitory effect, which was not a result of either the active transport or the metabolism of SAM. The quantitative recovery of labeled SAM from the incubation medium indicated that SAM, and not a metabolite, was the true inhibitory molecule. S-Adenosyl-L-homocysteine and S-adenosyl-L-ethionine also functioned as inhibitors of leucine transport, whereas S-adenosyl-D-methionine, S-adenosyl-D-homocystein, 5'-methylthioadenosine, 5'-dimethylthioadenosine, and adenosine lacked this property. Kinetic studies demonstrated that SAM was a competitive inhibitor of leucine transport.
S-腺苷-L-甲硫氨酸(SAM)抑制酿酒酵母中的亮氨酸转运。通过使用SAM主动转运缺陷的突变体,我们证明了抑制作用是在细胞外位点发挥的。用SAM预孵育120分钟的细胞对其抑制作用变得不敏感,这既不是SAM主动转运的结果,也不是其代谢的结果。从孵育培养基中定量回收标记的SAM表明,SAM而非代谢产物是真正的抑制分子。S-腺苷-L-高半胱氨酸和S-腺苷-L-乙硫氨酸也可作为亮氨酸转运的抑制剂,而S-腺苷-D-甲硫氨酸、S-腺苷-D-高半胱氨酸、5'-甲硫基腺苷、5'-二甲基硫代腺苷和腺苷则没有这种特性。动力学研究表明,SAM是亮氨酸转运的竞争性抑制剂。