Linder B, Harris S, Eisen A, Nissley P
Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.
Mol Cell Endocrinol. 1994 Oct;105(1):111-8. doi: 10.1016/0303-7207(94)90042-6.
A pertussis toxin-sensitive G protein has been reported to play a role in the mitogenic response to insulin-like growth factor-I (IGF-I) in mouse fibroblasts, and diacylglycerol generation has been shown to accompany growth stimulation by IGF-I of several cell lines. We have examined the roles of pertussis toxin sensitive G proteins and diacylglycerol generation in signaling by the insulin-like growth factor-I receptor in a cell line that is very responsive to IGF-I, the human osteosarcoma cell line, MG-63. Pertussis toxin failed to inhibit IGF-I induced [3H]-thymidine incorporation into DNA. Furthermore, the stable analog GTP gamma S had no effect on the binding of 125I-labelled IGF-I to MG-63 membrane preparations. Following addition of IGF-I to growth-arrested MG-63 cells there was no increase in diacylglycerol levels over 30 min. We conclude that the activated IGF-I receptor does not use pertussis toxin sensitive G proteins or diacylglycerol generation in a pathway leading to DNA synthesis in MG-63 cells.
据报道，一种对百日咳毒素敏感的G蛋白在小鼠成纤维细胞对胰岛素样生长因子-I（IGF-I）的促有丝分裂反应中起作用，并且已表明二酰基甘油的生成伴随着IGF-I对几种细胞系的生长刺激。我们已经在对IGF-I非常敏感的细胞系——人骨肉瘤细胞系MG-63中，研究了对百日咳毒素敏感的G蛋白和二酰基甘油生成在胰岛素样生长因子-I受体信号传导中的作用。百日咳毒素未能抑制IGF-I诱导的[3H] - 胸腺嘧啶核苷掺入DNA。此外，稳定类似物GTPγS对125I标记的IGF-I与MG-63细胞膜制剂的结合没有影响。在将IGF-I添加到生长停滞的MG-63细胞后，30分钟内二酰基甘油水平没有增加。我们得出结论，活化的IGF-I受体在导致MG-63细胞DNA合成的途径中不使用对百日咳毒素敏感的G蛋白或二酰基甘油生成。
