Song J G, Pfeffer L M, Foster D A
Institute for Biomolecular Structure and Function, Hunter College of The City University of New York.
Mol Cell Biol. 1991 Oct;11(10):4903-8. doi: 10.1128/mcb.11.10.4903-4908.1991.
Activating the protein-tyrosine kinase of v-Src in BALB/c 3T3 cells results in rapid increases in the intracellular second messenger, diacylglycerol (DAG). v-Src-induced increases in radiolabeled DAG were most readily detected when phospholipids were prelabeled with myristic acid, which is incorporated predominantly into phosphatidylcholine. Consistent with this observation, v-Src increased the level of intracellular choline. No increase in DAG was observed when cells were prelabeled with arachidonic acid, which is incorporated predominantly into phosphatidylinositol. Inhibiting phosphatidic acid (PA) phosphatase, which hydrolyzes PA to DAG, blocked v-Src-induced DAG production and enhanced PA production, implicating a type D phospholipase. Consistent with the involvement of a type D phospholipase, v-Src increased transphosphatidylation activity, which is characteristic of type D phospholipases. Thus, v-Src-induced increases in DAG most likely result from the activation of a type D phospholipase/PA phosphatase-mediated signaling pathway.
在BALB/c 3T3细胞中激活v-Src的蛋白酪氨酸激酶会导致细胞内第二信使二酰基甘油（DAG）迅速增加。当磷脂用肉豆蔻酸预标记时，v-Src诱导的放射性标记DAG增加最容易被检测到，肉豆蔻酸主要掺入磷脂酰胆碱中。与这一观察结果一致，v-Src增加了细胞内胆碱的水平。当细胞用花生四烯酸预标记时，未观察到DAG增加，花生四烯酸主要掺入磷脂酰肌醇中。抑制将磷脂酸（PA）水解为DAG的PA磷酸酶可阻断v-Src诱导的DAG产生并增强PA产生，这表明涉及D型磷脂酶。与D型磷脂酶的参与一致，v-Src增加了转磷脂酰基活性，这是D型磷脂酶的特征。因此，v-Src诱导的DAG增加很可能是由D型磷脂酶/PA磷酸酶介导的信号通路激活所致。
