Following cell stress, a wide range of molecular pathways are initiated to orchestrate the stress response and enable adaptation to an environmental or intracellular perturbation. The post-transcriptional regulation strategies adopted during the stress response result in a substantial reorganization of gene expression, designed to prepare the cell for either acclimatization or programmed death, depending on the nature and intensity of the stress. Fundamental to the stress response is a rapid repression of global protein synthesis, commonly mediated by phosphorylation of translation initiation factor eIF2α. Recent structural and biochemical information have added unprecedented detail to our understanding of the molecular mechanisms underlying this regulation. During protein synthesis inhibition, the translation of stress-specific mRNAs is nonetheless enhanced, often through the interaction between RNA-binding proteins and specific RNA regulatory elements. Recent studies investigating the unfolded protein response (UPR) provide some important insights into how posttranscriptional events are spatially and temporally fine-tuned in order to elicit the most appropriate response and to coordinate the transition from an early, acute stage into the chronic state of adaptation. Importantly, cancer cells are known to hi-jack adaptive stress response pathways, particularly the UPR, to survive and proliferate in the unfavorable tumor environment. In this review, we consider the implications of recent research into stress-dependent post-transcriptional regulation and make the case for the exploration of the stress response as a strategy to identify novel targets in the development of cancer therapies. This article is categorized under: RNA in Disease and Development > RNA in Disease RNA Evolution and Genomics > RNA and Ribonucleoprotein Evolution Translation > Translation Mechanisms > Translation Regulation.

中文翻译：

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细胞应激反应：极端的时候需要转录后的措施。

细胞应激后，广泛的分子途径被启动以协调应激反应并使其适应环境或细胞内扰动。在应激反应期间采用的转录后调控策略导致基因表达的实质性重组，旨在根据应激的性质和强度使细胞为适应环境或程序性死亡做好准备。应激反应的基础是快速抑制总体蛋白质合成，通常通过翻译起始因子eIF2α的磷酸化介导。最近的结构和生化信息为我们对这种调节基础的分子机理的理解增加了空前的细节。在蛋白质合成抑制过程中，但是，通常通过RNA结合蛋白与特定RNA调控元件之间的相互作用，增强了应力特异性mRNA的翻译。最近的研究展开蛋白反应（UPR）的研究为转录后事件如何在空间和时间上进行微调提供了重要的见解，以便引起最适当的反应并协调从早期，急性阶段到慢性适应状态的转变。重要的是，已知癌细胞会劫持适应性应激反应途径，特别是UPR，以在不利的肿瘤环境中生存和增殖。在这篇评论中 我们考虑了最近对应激依赖性转录后调控研究的意义，并为探讨应激反应作为鉴定癌症治疗发展中新靶点的策略提供了理由。本文归类于：疾病与发展中的RNA>疾病中的RNA RNA进化与基因组学> RNA与核糖核蛋白进化翻译>翻译机制>翻译调控。