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低温诱导的小鼠组织细胞应激反应的特征

Characterization of hypothermia-induced cellular stress response in mouse tissues.

作者信息

Cullen K E, Sarge K D

机构信息

Department of Biochemistry, Chandler Medical Center, University of Kentucky, Lexington, Kentucky 40536-0084, USA.

出版信息

J Biol Chem. 1997 Jan 17;272(3):1742-6. doi: 10.1074/jbc.272.3.1742.

Abstract

Cells respond to adverse environmental conditions by expressing heat shock proteins, which serve to protect cells from harmful effects of the stress conditions. In this study we demonstrated that mice subjected to whole body hypothermia induced the cellular stress response, resulting in the increased expression of hsp72 mRNA in brain, heart, kidney, liver, and lung. We performed a detailed analysis of the major parameters of the stress response and found that cold induction of hsp expression is mediated by heat shock factor 1 (HSF1), which is also responsible for heat induction of the cellular stress response. However, there are differences in the mechanisms of HSF1 activation by hypothermia versus hyperthermia, as hypothermia does not cause the hyperphosphorylation of HSF1 that is characteristic of heat-activated HSF1.

摘要

细胞通过表达热休克蛋白来应对不利的环境条件,热休克蛋白有助于保护细胞免受应激条件的有害影响。在本研究中,我们证明,遭受全身低温的小鼠会诱导细胞应激反应,导致脑、心脏、肾脏、肝脏和肺中hsp72 mRNA表达增加。我们对应激反应的主要参数进行了详细分析,发现hsp表达的冷诱导是由热休克因子1(HSF1)介导的,HSF1也负责细胞应激反应的热诱导。然而,低温与高温激活HSF1的机制存在差异,因为低温不会导致热激活HSF1所特有的HSF1超磷酸化。

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