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Transformation by the src oncogene alters glucose transport into rat and chicken cells by different mechanisms.

机译:src癌基因的转化通过不同的机制改变了葡萄糖向大鼠和鸡细胞的转运。

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摘要

Transformation of both rat and chicken fibroblasts by the src oncogene leads to a four- to fivefold increase in the rate of glucose transport and in the level of the glucose transporter protein. We have previously shown that, with chicken embryo fibroblasts, transformation leads to a reduction in the rate of degradation of the transporter, with little or no increase in the rate of its biosynthesis. We now show that, with the rat-1 cell line, the opposite result was obtained. src-induced transformation led to an increase in transporter biosynthesis, with little effect on turnover. A src-induced increase in transporter mRNA entirely accounted for the increase in biosynthesis of the protein. By contrast, in chicken embryo fibroblasts, the level of transporter mRNA was low and was not induced to rise by src transformation. Thus, src induced an increase in the level of the glucose transport protein by fundamentally different mechanisms in chicken embryo fibroblasts and rat-1 cells. To test whether this difference was due to rat-1 cells being an immortalized cell line, we measured transporter mRNA levels in primary fibroblast cultures from rat embryos and in parallel cultures transformed by src. Transporter mRNA was inducible by src in these cells. Thus, the difference in mRNA inducibility between chicken and rat cells is not due to immortalization.
机译:src致癌基因对大鼠和鸡成纤维细胞的转化导致葡萄糖转运速率和葡萄糖转运蛋白水平增加了四到五倍。先前我们已经表明,对于鸡胚成纤维细胞,转化导致转运蛋白降解速率降低,而其生物合成速率几乎没有增加。现在我们显示,使用rat-1细胞系,可获得相反的结果。 src诱导的转化导致转运蛋白生物合成的增加,对营业额的影响很小。 src诱导的转运蛋白mRNA的增加完全解释了蛋白质生物合成的增加。相比之下,在鸡胚成纤维细胞中,转运蛋白的mRNA水平较低,并且不会通过src转化诱导其升高。因此,src通过根本不同的机制诱导了鸡胚成纤维细胞和rat-1细胞中葡萄糖转运蛋白水平的增加。为了测试这种差异是否归因于大鼠1细胞是永生的细胞系,我们测量了来自大鼠胚胎的原代成纤维细胞培养物中以及由src转化的平行培养物中转运蛋白的mRNA水平。转运蛋白mRNA可在这些细胞中被src诱导。因此,鸡和大鼠细胞之间mRNA诱导能力的差异并不是由于永生化。

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