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化学应激不会诱导利什曼原虫中的热休克蛋白合成。

Chemical Stress does not Induce Heat Shock Protein Synthesis in Leishmania donovani.

机构信息

Bernhard Nocht Institute for Tropical Medicine, Bernhard Nocht St. 74, D-20359 Hamburg, Germany.

出版信息

Protist. 1998 May;149(2):167-72. doi: 10.1016/S1434-4610(98)70021-5. Epub 2009 Jul 13.

Abstract

The cellular heat shock response in kinetoplastid protozoa is regulated exclusively at a post-transcriptional level. The heat-inducibility of heat shock protein synthesis is retained under actinomycin C(1) which indicates an inducible translation of heat shock mRNAs. We have also assessed the ability of various chemicals known to be effective triggers of the heat shock response in higher eukaryotes to induce heat shock protein synthesis in Leishmania donovani. None of the tested chemicals elicited a stress response. We propose that the lack of transcription regulation in the kinetoplastida precludes a stress response under chemical stress.

摘要

动基体原虫中的细胞热休克反应仅在转录后水平受到调节。在放线菌素 C(1)的作用下,热休克蛋白合成的热诱导性得以保留,这表明热休克 mRNAs 可进行诱导翻译。我们还评估了各种已知可有效引发高等真核生物热休克反应的化学物质在杜氏利什曼原虫中诱导热休克蛋白合成的能力。测试的化学物质均未引起应激反应。我们提出,动基体原虫中缺乏转录调控使得它们在化学应激下无法产生应激反应。

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