HEAT-SHOCK PROTEIN HSP70 ACCELERATES THE RECOVERY OF HEAT-SHOCKED MAMMALIAN-CELLS THROUGH ITS MODULATION OF HEAT-SHOCK TRANSCRIPTION FACTOR HSF1

HEAT-SHOCK PROTEIN HSP70 ACCELERATES THE RECOVERY OF HEAT-SHOCKED MAMMALIAN-CELLS THROUGH ITS MODULATION OF HEAT-SHOCK TRANSCRIPTION FACTOR HSF1
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DOI:
10.1073/pnas.92.6.2126
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发表时间:
1995-03-14
影响因子:
11.1
通讯作者:
LI, GC
LI, GC
中科院分区:
综合性期刊1区
文献类型:
--
作者:
KIM, DH;OUYANG, H;LI, GC

文献摘要

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哺乳动物70-kDa热休克蛋白(hsp 70)在调节细胞对热休克的反应中的作用通过使用三种密切相关的大鼠细胞来检测:对照大鼠-1细胞,耐热大鼠-1(TT Rat-1)细胞和耐热M21细胞,耐热M21细胞是组成型过表达人hsp 70的Rat-1细胞的衍生物。在所有这些细胞中,在规定的热休克后,磷酸化形式的热休克转录因子HSF 1的水平和能够结合其认知DNA序列热休克元件(HSE)的HSF 1的水平表现出类似的时间依赖性。另一方面,组成型HSE结合活性(CHBA)的量与前述两种形式的HSF 1的量负相关。三种细胞系的热休克恢复动力学不同,耐热TT Rat-1和M21细胞在HSF 1磷酸化状态及其结合HSE的能力方面或在CHBA重现方面显示出更快的恢复。冈田酸,丝氨酸/苏氨酸磷酸酶抑制剂,治疗延迟Rat-1细胞的恢复动力学,但不是耐热的M21细胞,这些结果被解释在热休克哺乳动物细胞的恢复中的作用。
The role of mammalian 70-kDa heat shock protein (hsp70) in regulating cellular response to heat shock was examined by using three closely related rat cells: control Rat-1 cells, thermotolerant Rat-1 (TT Rat-1) cells, and heat-resistant M21 cells, a derivative of Rat-1 cells that constitutively overexpress human hsp70, In all these cells, after a prescribed heat shock, the level of the phosphorylated form of heat shock transcription factor HSF1 and that of HSF1 capable of binding to its cognitive DNA sequence heat shock element (HSE) exhibit similar time dependence. The amount of a constitutive HSE-binding activity (CHBA), on the other hand, inversely correlates with those of the two aforementioned forms of HSF1. The recovery kinetics from heat shock are different for the three cell lines, with the thermal-resistant TT Rat-1 and M21 cells showing faster recovery in terms of the state of phosphorylation of HSF1 and its ability to bind HSE or in terms of the reappearance of CHBA. Treatment with okadaic acid, a serine/threonine phosphatase inhibitor, delays the recovery kinetics of Rat-1 cells but not that of thermal-resistant M21 cells, These results are interpreted in terms of a role for hsp70 in the recovery of heat-shocked mammalian cells.