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缺乏泛素激活酶的小鼠温度敏感突变体ts85热耐受性发育缺陷。

Defect in the development of thermotolerance in the mouse temperature-sensitive mutant ts85 lacking ubiquitin-activating enzyme.

作者信息

Mizuno S, Ohkawara A, Suzuki K

机构信息

Department of Antibiotics, National Institute of Health, Tokyo.

出版信息

Jpn J Cancer Res. 1988 Jan;79(1):17-20. doi: 10.1111/j.1349-7006.1988.tb00005.x.

Abstract

We investigated the effect of heat shock on the development of thermotolerance using mouse FM3A cells and the temperature-sensitive mutant ts85. The shift-up incubation of FM3A from 33 to 39.5 degrees induced thermotolerance to subsequent heating at 44 degrees. In contrast, the similar treatment of ts85 at the nonpermissive temperature of 39.5 degrees could not induce thermotolerance. Furthermore, when ts85 cells were treated at 33 degrees after being heated at 44 degrees, they developed a reduced level of thermotolerance as compared with that developed in FM3A cells. Since ts85 cells are defective in ubiquitin-activating enzyme, these results suggest a role of the ubiquitin-protein conjugation system in the development of thermotolerance.

摘要

我们使用小鼠FM3A细胞和温度敏感突变体ts85研究了热休克对耐热性发展的影响。将FM3A从33℃向上转移至39.5℃培养可诱导其对随后44℃加热产生耐热性。相比之下,在39.5℃的非允许温度下对ts85进行类似处理不能诱导耐热性。此外,当ts85细胞在44℃加热后于33℃处理时,与FM3A细胞相比,它们产生的耐热性水平降低。由于ts85细胞在泛素激活酶方面存在缺陷,这些结果表明泛素-蛋白质缀合系统在耐热性发展中起作用。

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本文引用的文献

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The stress response: changes in eukaryotic gene expression in response to environmental stress.
Science. 1985 Nov 15;230(4727):800-1. doi: 10.1126/science.230.4727.800-a.
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Mechanisms of intracellular protein breakdown.细胞内蛋白质降解的机制。
Annu Rev Biochem. 1982;51:335-64. doi: 10.1146/annurev.bi.51.070182.002003.
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Ubiquitin - protein conjugates.泛素-蛋白质缀合物
Mol Cell Biochem. 1981 Nov 13;40(3):173-87. doi: 10.1007/BF00224611.

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