ANTIPROLIFERATIVE PROSTAGLANDINS ACTIVATE HEAT-SHOCK TRANSCRIPTION FACTOR
ANTIPROLIFERATIVE PROSTAGLANDINS ACTIVATE HEAT-SHOCK TRANSCRIPTION FACTOR
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DOI：
10.1073/pnas.89.14.6227
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发表时间：
1992-07-15
影响因子：
11.1
通讯作者：
MORIMOTO, RI
中科院分区：
文献类型：
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作者：
AMICI, C;SISTONEN, L;MORIMOTO, RI
用抗增殖前列腺素A1处理人K562红白血病细胞导致两种热休克基因HSP 70和HSP 90的转录升高。与热休克基因转录增加平行的是热休克转录因子的激活。热休克转录因子水平在前列腺素A1添加后60分钟内诱导至与热休克期间达到的水平相似的水平。前列腺素A1激活热休克转录因子的蛋白质合成的要求表明，对新生蛋白质合成的影响可能涉及的信号传导机制。虽然目前还不清楚是否激活热休克反应的mesylandins是相关的生化性质，这些天然物质，细胞预处理与前列腺素A1的保护，防止随后的热休克，表明一个耐热状态。
Treatment of human K562 erythroleukemia cells with the antiproliferative prostaglandin A1 results in the elevated transcription of two heat shock genes, HSP70 and HSP90. Parallel with increased heat shock gene transcription is the activation of heat shock transcription factor. Heat shock transcription factor levels are induced within 60 min after prostaglandin A1 addition to levels similar to that achieved during heat shock. The requirement for protein synthesis for prostaglandin A1 activation of heat shock transcription factor suggests that effects on nascent protein synthesis may be involved in the signaling mechanism. Although it is unclear whether the activation of a heat shock response by prostaglandins is relevant to the biochemical properties of these natural substances, cells pretreated with prostaglandin A1 are protected against a subsequent heat shock, indicative of a thermotolerant state.