Párrizas M, Gazit A, Levitzki A, Wertheimer E, LeRoith D
Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892, USA.
Endocrinology. 1997 Apr;138(4):1427-33. doi: 10.1210/endo.138.4.5092.
A series of the synthetic protein tyrosine kinase inhibitors known as tyrphostins were studied for their effect on insulin-like growth factor-1 and insulin-stimulated cellular proliferation on NIH-3T3 fibroblasts overexpressing either receptor, as well as for their ability to inhibit ligand-stimulated receptor autophosphorylation and tyrosine kinase activity toward exogenous substrates. Several of the tyrphostins tested demonstrated a dramatic effect by inhibiting hormone-stimulated cell proliferation, with IC50s in the submicromolar range, while being unable to block serum-stimulated cell proliferation. The tyrphostins also inhibited receptor autophosphorylation and tyrosine kinase activity, with a higher IC50, in the micromolar range. Most of the tyrphostins tested presented no clear preference for either receptor, although two of them (AG1024 and AG1034) showed significantly lower IC50s for IGF-1 than for insulin receptors. These results suggest that, in spite of the high homology of the kinase regions of both receptors, it could be possible to design and synthesize small molecules capable of discriminating between them. The synthesis of such specific inhibitors could be an excellent tool to establish the precise signalling mechanisms that distinguish between the different effects of these two hormones.
研究了一系列称为 tyrphostins 的合成蛋白酪氨酸激酶抑制剂,考察它们对过表达胰岛素样生长因子-1(IGF-1)受体或胰岛素受体的 NIH-3T3 成纤维细胞中 IGF-1 和胰岛素刺激的细胞增殖的影响,以及它们抑制配体刺激的受体自身磷酸化和对外源底物的酪氨酸激酶活性的能力。所测试的几种 tyrphostins 通过抑制激素刺激的细胞增殖显示出显著效果,IC50 在亚微摩尔范围内,而无法阻断血清刺激的细胞增殖。tyrphostins 还抑制受体自身磷酸化和酪氨酸激酶活性,IC50 较高,在微摩尔范围内。大多数所测试的 tyrphostins 对两种受体均无明显偏好,尽管其中两种(AG1024 和 AG1034)对 IGF-1 受体的 IC50 比对胰岛素受体的显著更低。这些结果表明,尽管两种受体的激酶区域具有高度同源性,但仍有可能设计和合成能够区分它们的小分子。合成此类特异性抑制剂可能是确立区分这两种激素不同效应的精确信号传导机制的极佳工具。