Mechanisms of activation and regulation of the heat shock-sensitive signaling pathways.
Mechanisms of activation and regulation of the heat shock-sensitive signaling pathways.
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DOI：
10.1007/978-0-387-39975-1_10
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发表时间：
2007
影响因子：
--
通讯作者：
Sébastien Nadeau;J. Landry
中科院分区：
文献类型：
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作者：
Sébastien Nadeau;J. Landry
热休克（HS），像许多其他的压力，诱导特定的和高度调节的信号级联，促进细胞内稳态。三种主要的促分裂原活化蛋白激酶（MAPK）和蛋白激酶B（PKB/Akt）是这些HS刺激的途径中最显著的。它们的激活发生迅速，比热休克蛋白（HSP）的转录上调更快，热休克蛋白产生对随后的热应激的极端抗性的瞬时状态。这些信号通路与细胞死亡或存活机制的直接联系表明它们对HS反应有重要贡献。它们中的一些可能抵消热的早期有害影响，而另一些可能支持关键的凋亡事件。负责激活这些通路的触发事件尚不清楚。蛋白质变性、特异性和非特异性受体激活、膜改变和染色质结构扰动是潜在的启动因子。
Heat shock (HS), like many other stresses, induces specific and highly regulated signaling cascades that promote cellular homeostasis. The three major mitogen-activated protein kinases (MAPK) and protein kinase B (PKB/Akt) are the most notable of these HS-stimulated pathways. Their activation occurs rapidly and sooner than the transcriptional upregulation of heat shock proteins (Hsp), which generate a transient state of extreme resistance against subsequent thermal stress. The direct connection of these signaling pathways to cellular death or survival mechanisms suggests that they contribute importantly to the HS response. Some of them may counteract early noxious effects of heat, while others may bolster key apoptosis events. The triggering events responsible for activating these pathways are unclear. Protein denaturation, specific and nonspecific receptor activation, membrane alteration and chromatin structure perturbation are potential initiating factors.