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v-Src increases diacylglycerol levels via a type D phospholipase-mediated hydrolysis of phosphatidylcholine.

机译:v-Src通过D型磷脂酶介导的磷脂酰胆碱水解增加二酰基甘油水平。

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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.
机译: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种信使二酰基甘油(DAG)迅速增加。当用肉豆蔻酸预先标记磷脂时,v-Src诱导的放射性标记DAG的增加最容易检测到,而肉豆蔻酸主要掺入磷脂酰胆碱中。与该观察结果一致,v-Src增加了细胞内胆碱的水平。当用花生四烯酸预先标记细胞时,未观察到DAG的增加,花生四烯酸主要掺入磷脂酰肌醇。抑制磷脂酸(PA)的磷酸酶将PA水解为DAG,可阻止v-Src诱导的DAG产生并增强PA的产生,这涉及D型磷脂酶。与D型磷脂酶的参与一致,v-Src增加了转磷酸酯化活性,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磷酸酶介导的信号传导途径的激活引起的。

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