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Degradation and biosynthesis of the glucose transporter protein in chicken embryo fibroblasts transformed by the src oncogene.

机译:src致癌基因转化的鸡胚成纤维细胞中葡萄糖转运蛋白的降解和生物合成。

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摘要

The rate of glucose transport in cultured fibroblasts is regulated to a number of physiological variables, including malignant transformation by src, glucose starvation, and stimulation with mitogens. Much of this transport regulation can be accounted for by variations in the amount of transporter protein in the cells. To determine the mechanisms by which levels of the transporter are regulated, we measured the rates of synthesis and degradation of the transporter by pulse-chase experiments and immunoprecipitation of the transporter. We found that transformation by the src oncogene results in a large decrease in the rate at which the transporter protein is degraded but that it does not appreciably increase the rate of transporter biosynthesis. On the other hand, glucose starvation and mitogen stimulation increase the rate of transporter biosynthesis, although a role for control of degradation is possible in these circumstances also. Variations in the rate of glucose transport or the amount of the transporter are not associated with phosphorylation of the transporter protein.
机译:培养的成纤维细胞中葡萄糖的转运速率受许多生理变量的调节,包括src引起的恶性转化,葡萄糖饥饿和促有丝分裂原刺激。这种转运调节的大部分可以通过细胞中转运蛋白数量的变化来解释。为了确定调节转运蛋白水平的机制,我们通过脉冲追踪实验和转运蛋白的免疫沉淀法测量了转运蛋白的合成和降解速率。我们发现由src致癌基因转化导致转运蛋白降解的速率大大降低,但并未显着提高转运蛋白生物合成的速率。另一方面,尽管在这些情况下也有控制降解的作用,但葡萄糖饥饿和促有丝分裂原刺激可提高转运蛋白的生物合成速率。葡萄糖转运速率或转运蛋白数量的变化与转运蛋白的磷酸化无关。

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