Körner C, Braulke T
Institute of Biochemistry II, University of Göttingen, Germany.
Mol Cell Endocrinol. 1996 Apr 19;118(1-2):201-5. doi: 10.1016/0303-7207(96)03785-9.
The effects of wortmannin, a selective inhibitor of phosphatidylinositol (PI)3-kinase on insulin-like growth factor II (IGF II)-induced redistribution of the 300 kDa mannose 6-phosphate/IGF II receptor (MPR 300) has been studied in human hepatoma HepG2 cells. IGF II increased the expression of MPR 300 at the cell surface threefold that was completely abolished by wortmannin at 100-300 nM. Higher concentrations of wortmannin also reduced the basal MPR 300-dependent uptake of ligands to 68% of controls. Neither the transport of two lysosomal enzymes nor the secretion of the IGF binding protein-1 were affected by wortmannin. These results show that activation of PI3-kinase plays a critical role in the IGF II-stimulated redistribution of MPR 300 initiated rather by IGF II binding to tyrosine kinase receptors than to the MPR 300.
在人肝癌HepG2细胞中，研究了磷脂酰肌醇（PI）3激酶的选择性抑制剂渥曼青霉素对胰岛素样生长因子II（IGF II）诱导的300 kDa甘露糖6磷酸/IGF II受体（MPR 300）重新分布的影响。IGF II使细胞表面MPR 300的表达增加了三倍，而在100 - 300 nM的渥曼青霉素可完全消除这种增加。更高浓度的渥曼青霉素也将依赖MPR 300的配体基础摄取量降低至对照的68%。渥曼青霉素既不影响两种溶酶体酶的转运，也不影响IGF结合蛋白-1的分泌。这些结果表明，PI3激酶的激活在IGF II刺激的MPR 300重新分布中起关键作用，这种重新分布更多是由IGF II与酪氨酸激酶受体结合而非与MPR 300结合引发的。
