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钙缺乏大鼠肝癌细胞中热休克反应的抑制及葡萄糖调节蛋白的合成

Inhibition of the heat shock response and synthesis of glucose-regulated proteins in Ca2+-deprived rat hepatoma cells.

作者信息

Lamarche S, Chrétien P, Landry J

出版信息

Biochem Biophys Res Commun. 1985 Sep 16;131(2):868-76. doi: 10.1016/0006-291x(85)91320-8.

Abstract

Rat hepatoma cells become refractory to the induction of heat shock proteins and highly resistant to severe hyperthermia when incubated in Ca2+-free medium. The Ca2+-depleted cells synthesize polypeptides identified as the glucose-regulated proteins, but these proteins do not appear to be directly involved in the inhibition of the heat shock response. The results suggest that a Ca2+-dependent metabolic process is involved in the generation of the heat shock signal and/or mediates a step in the subsequent cascade of events that leads to the induction of heat shock protein synthesis and cell death.

摘要

当在无钙培养基中培养时,大鼠肝癌细胞对热休克蛋白的诱导变得不敏感,并且对严重高热具有高度抗性。缺钙的细胞合成被鉴定为葡萄糖调节蛋白的多肽,但这些蛋白似乎并未直接参与热休克反应的抑制。结果表明,一个依赖钙的代谢过程参与了热休克信号的产生和/或介导了随后导致热休克蛋白合成诱导和细胞死亡的一系列事件中的一个步骤。

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