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耐受过程中热休克蛋白的重新诱导是否与应激源特异性诱导热休克蛋白有关?

Is heat shock protein re-induction during tolerance related to the stressor-specific induction of heat shock proteins?

作者信息

Wiegant F A, Spieker N, Van der Mast C A, Van Wijk R

机构信息

Department of Molecular Cell Biology, Utrecht University, The Netherlands.

出版信息

J Cell Physiol. 1996 Nov;169(2):364-72. doi: 10.1002/(SICI)1097-4652(199611)169:2<364::AID-JCP16>3.0.CO;2-9.

Abstract

The existence of stressor-specific induction programs of heat shock proteins (hsps) leads us to analyze the possible occurrence of a stressor-specific tolerance induced by either heat shock, arsenite, or cadmium. As a measure of this tolerance re-induction of hsps was studied. In this paper, we tested whether the refractory state is either valid for each specific hsp (implying independent regulation of every member of the heat shock protein family) or extends from small subsets of the hsp-family to even larger groups of proteins (indicating a more common denominator in their regulation). (re-)induction of hsps does not seem to be regulated at the level of each individual hsp since differences in induced synthesis of hsps between two stressor conditions are not supplemented systematically upon the sequential application of the two stressors. The most notable example in this respect is hsp60. A pretreatment with cadmium, which hardly induces synthesis of this hsp, does induce a tolerance to (re)-induction by heat shock, which normally induces hsp60. This suggests the existence of a more common denominator regulating the coordinate expression of at least some hsps. From our data we conclude that the degree, but not the pattern, of hsp re-induction is influenced by the type of stressor used in the pretreatment. The pattern of hsps induced by a secondary applied stressor still shows most of its stressor-specificity and seems to be independent of any pretreatment. The possible implications of stressor-specificity are discussed.

摘要

热休克蛋白(hsps)应激源特异性诱导程序的存在促使我们分析由热休克、亚砷酸盐或镉诱导的应激源特异性耐受性的可能发生情况。作为这种耐受性的一种衡量方法,我们研究了热休克蛋白的重新诱导情况。在本文中,我们测试了不应期状态是对每个特定的热休克蛋白都有效(这意味着热休克蛋白家族的每个成员都有独立的调节机制),还是从热休克蛋白家族的小子集扩展到更大的蛋白质组(这表明它们在调节方面有更普遍的共同特征)。热休克蛋白的(重新)诱导似乎不是在每个单独的热休克蛋白水平上进行调节的,因为在两种应激源条件下热休克蛋白诱导合成的差异在依次施加这两种应激源时并没有系统地得到补充。在这方面最显著的例子是hsp60。用镉进行预处理,镉几乎不诱导这种热休克蛋白的合成,但却能诱导对通常诱导hsp60的热休克(重新)诱导产生耐受性。这表明存在一种更普遍的共同特征调节至少一些热休克蛋白的协同表达。从我们的数据中我们得出结论,热休克蛋白重新诱导的程度而非模式受到预处理中使用的应激源类型的影响。二次施加应激源诱导的热休克蛋白模式仍然显示出其大部分应激源特异性,并且似乎独立于任何预处理。我们讨论了应激源特异性的可能影响。

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