Heat shock factors and the control of the stress response
Heat shock factors and the control of the stress response
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DOI：
10.1016/s0006-2952(99)00299-3
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发表时间：
2000-01-01
影响因子：
5.8
通讯作者：
Santoro, MG
中科院分区：
文献类型：
--
作者：
Santoro, MG
活细胞不断受到引起急性和慢性应激的条件的挑战。为了适应环境变化和不同类型的损伤，真核细胞已经进化出不同的反应网络，可以检测和控制不同形式的压力。这些反应之一，被称为热休克反应，已经吸引了大量的关注，作为一个普遍的基本机制，细胞生存所必需的各种不利条件下。在哺乳动物细胞中，热休克反应的诱导需要一种或多种热休克转录因子的激活和易位到细胞核，所述热休克转录因子控制编码细胞保护性热休克蛋白的特定基因组的表达。热休克反应在几种病理条件下开启，并有助于在各种人类疾病（包括缺血、炎症和感染）中建立细胞保护状态，这一发现为医学和药理学开辟了新的视角，因为激活这种防御机制的分子似乎是新型细胞保护药物的可能候选者。本文重点介绍哺乳动物细胞中热休克反应的调控和功能，并讨论了应激和生物活性环戊烯酮前列腺素类激活热休克反应的分子机制，以及热休克反应与核因子KB的相互作用，核因子KB是一种应激调节的转录因子，在炎症和免疫中起着关键作用。生物化学制药59;1：55-63，2000年。(C)1999 Elsevier Science Inc.
Living cells are continually challenged by conditions which cause acute and chronic stress. To adapt to environmental changes and survive different types of injuries, eukaryotic cells have evolved networks of different responses which detect and control diverse forms of stress. One of these responses, known as the heat shock response, has attracted a great deal of attention as a universal fundamental mechanism necessary for cell survival under a variety of unfavorable conditions. In mammalian cells, the induction of the heat shock response requires the activation and translocation to the nucleus of one or more heat shock transcription factors which control the expression of a specific set of genes encoding cytoprotective heat shock proteins. The discovery that the heat shock response is turned on under several pathological conditions and contributes to establish a cytoprotective state in a variety of human diseases, including ischemia, inflammation, and infection, has opened new perspectives in medicine and pharmacology, as molecules activating this defense mechanism appear as possible candidates for novel cytoprotective drugs. This article focuses on the regulation and function of the heat shock response in mammalian cells and discusses the molecular mechanisms involved in its activation by stress and bioactive cyclopentenone prostanoids, as well as its interaction with nuclear factor KB, a stress-regulated transcription factor with a pivotal role in inflammation and immunity. BIOCHEM PHARMACOL 59;1:55-63, 2000. (C) 1999 Elsevier Science Inc.