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本文引用的文献

1
Playing the end game: DNA double-strand break repair pathway choice.玩终局游戏:DNA 双链断裂修复途径的选择。
Mol Cell. 2012 Aug 24;47(4):497-510. doi: 10.1016/j.molcel.2012.07.029.
2
BRCA1 and HSP90 cooperate in homologous and non-homologous DNA double-strand-break repair and G2/M checkpoint activation.BRCA1 和 HSP90 合作参与同源和非同源 DNA 双链断裂修复以及 G2/M 检查点激活。
Proc Natl Acad Sci U S A. 2012 Aug 21;109(34):13650-5. doi: 10.1073/pnas.1203326109. Epub 2012 Aug 6.
3
Hyperthermia-induced DNA repair deficiency suggests novel therapeutic anti-cancer strategies.热诱导的 DNA 修复缺陷提示了新型抗癌治疗策略。
Int J Hyperthermia. 2012;28(6):509-17. doi: 10.3109/02656736.2012.695427. Epub 2012 Jul 26.
4
Nucleotide excision repair: new tricks with old bricks.核苷酸切除修复:旧砖新用。
Trends Genet. 2012 Nov;28(11):566-73. doi: 10.1016/j.tig.2012.06.004. Epub 2012 Jul 22.
5
Dual effect of heat shock on DNA replication and genome integrity.热休克对 DNA 复制和基因组完整性的双重影响。
Mol Biol Cell. 2012 Sep;23(17):3450-60. doi: 10.1091/mbc.E11-12-1009. Epub 2012 Jul 11.
6
Inhibition of HSP70: a challenging anti-cancer strategy.抑制 HSP70:一项具有挑战性的抗癌策略。
Cancer Lett. 2012 Dec 28;325(2):117-24. doi: 10.1016/j.canlet.2012.06.003. Epub 2012 Jun 28.
7
Hyperthermia induces cytoskeletal alterations and mitotic catastrophe in p53-deficient H1299 lung cancer cells.高热诱导 p53 缺陷型 H1299 肺癌细胞骨架改变和有丝分裂灾难。
Acta Histochem. 2013 Jan;115(1):8-15. doi: 10.1016/j.acthis.2012.02.006. Epub 2012 Apr 6.
8
The heat shock response: systems biology of proteotoxic stress in aging and disease.热休克反应:衰老与疾病中蛋白质毒性应激的系统生物学
Cold Spring Harb Symp Quant Biol. 2011;76:91-9. doi: 10.1101/sqb.2012.76.010637. Epub 2012 Feb 27.
9
Ferruccio Ritossa's scientific legacy 50 years after his discovery of the heat shock response: a new view of biology, a new society, and a new journal.费鲁乔·里托萨(Ferruccio Ritossa)发现热休克反应 50 年后的科学遗产:生物学的新视角、新社会和新期刊。
Cell Stress Chaperones. 2012 Mar;17(2):139-43. doi: 10.1007/s12192-012-0320-z. Epub 2012 Jan 18.
10
Inhibition of checkpoint kinase 1 abrogates G2/M checkpoint activation and promotes apoptosis under heat stress.抑制检查点激酶 1 可破坏热应激下的 G2/M 检查点激活并促进细胞凋亡。
Apoptosis. 2012 Jan;17(1):102-12. doi: 10.1007/s10495-011-0660-7.

哺乳动物热休克反应的机制。

Mechanisms of heat shock response in mammals.

机构信息

Laboratory of Structural and Functional Organization of Chromosomes, Institute of Gene Biology, Russian Academy of Sciences, 119334, Moscow, Russia.

出版信息

Cell Mol Life Sci. 2013 Nov;70(22):4229-41. doi: 10.1007/s00018-013-1348-7. Epub 2013 Apr 30.

DOI:10.1007/s00018-013-1348-7
PMID:23633190
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11113869/
Abstract

Heat shock (HS) is one of the best-studied exogenous cellular stresses. The cellular response to HS utilizes ancient molecular networks that are based primarily on the action of stress-induced heat shock proteins and HS factors. However, in one way or another, all cellular compartments and metabolic processes are involved in such a response. In this review, we aimed to summarize the experimental data concerning all aspects of the HS response in mammalian cells, such as HS-induced structural and functional alterations of cell membranes, the cytoskeleton and cellular organelles; the associated pathways that result in different modes of cell death and cell cycle arrest; and the effects of HS on transcription, splicing, translation, DNA repair, and replication.

摘要

热休克 (HS) 是研究最为广泛的外源性细胞应激之一。细胞对热休克的反应利用了古老的分子网络,主要基于应激诱导的热休克蛋白和 HS 因子的作用。然而,无论以何种方式,所有的细胞区室和代谢过程都参与了这种反应。在这篇综述中,我们旨在总结有关哺乳动物细胞热休克反应各个方面的实验数据,如热休克诱导的细胞膜、细胞骨架和细胞器的结构和功能改变;导致不同细胞死亡和细胞周期阻滞模式的相关途径;以及热休克对转录、剪接、翻译、DNA 修复和复制的影响。