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本文引用的文献

1
Altered chromatin architecture underlies progressive impairment of the heat shock response in mouse models of Huntington disease.染色质结构的改变是亨廷顿病小鼠模型中热休克反应进行性损伤的基础。
J Clin Invest. 2011 Aug;121(8):3306-19. doi: 10.1172/JCI57413. Epub 2011 Jul 25.
2
Huntington's disease: can mice lead the way to treatment?亨廷顿病:老鼠能为治疗指明方向吗?
Neuron. 2011 Feb 10;69(3):423-35. doi: 10.1016/j.neuron.2010.12.035.
3
Protein homeostasis and the phenotypic manifestation of genetic diversity: principles and mechanisms.蛋白质平衡和遗传多样性的表型表现:原理和机制。
Annu Rev Genet. 2010;44:189-216. doi: 10.1146/annurev.genet.40.110405.090412.
4
Emergence and natural selection of drug-resistant prions.耐药性朊病毒的出现与自然选择
Mol Biosyst. 2010 Jul;6(7):1115-30. doi: 10.1039/c004550k. Epub 2010 Apr 27.
5
Prion-like disorders: blurring the divide between transmissibility and infectivity.朊病毒样疾病:传染性与感染性之间的界限日益模糊。
J Cell Sci. 2010 Apr 15;123(Pt 8):1191-201. doi: 10.1242/jcs.051672.
6
Modulation of heat shock transcription factor 1 as a therapeutic target for small molecule intervention in neurodegenerative disease.作为神经退行性疾病中小分子干预治疗靶点的热休克转录因子 1 的调节。
PLoS Biol. 2010 Jan 19;8(1):e1000291. doi: 10.1371/journal.pbio.1000291.
7
Distinct conformations of in vitro and in vivo amyloids of huntingtin-exon1 show different cytotoxicity.亨廷顿蛋白外显子1的体外和体内淀粉样蛋白的不同构象表现出不同的细胞毒性。
Proc Natl Acad Sci U S A. 2009 Jun 16;106(24):9679-84. doi: 10.1073/pnas.0812083106. Epub 2009 Jun 1.
8
Biological and chemical approaches to diseases of proteostasis deficiency.针对蛋白质稳态缺陷相关疾病的生物学和化学方法。
Annu Rev Biochem. 2009;78:959-91. doi: 10.1146/annurev.biochem.052308.114844.
9
Impaired ERAD and ER stress are early and specific events in polyglutamine toxicity.内质网相关蛋白降解功能受损和内质网应激是多聚谷氨酰胺毒性中的早期特异性事件。
Genes Dev. 2008 Dec 1;22(23):3308-19. doi: 10.1101/gad.1673408. Epub 2008 Nov 17.
10
Chemical and biological approaches synergize to ameliorate protein-folding diseases.化学和生物学方法协同作用以改善蛋白质折叠疾病。
Cell. 2008 Sep 5;134(5):769-81. doi: 10.1016/j.cell.2008.06.037.

震惊与敬畏:释放热休克反应以治疗亨廷顿病。

Shock and awe: unleashing the heat shock response to treat Huntington disease.

出版信息

J Clin Invest. 2011 Aug;121(8):2972-5. doi: 10.1172/JCI59190. Epub 2011 Jul 25.

DOI:10.1172/JCI59190
PMID:21785212
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3148752/
Abstract

The heat shock response (HSR) is a highly conserved protective mechanism that enables cells to withstand diverse environmental stressors that disrupt protein homeostasis (proteostasis) and promote protein misfolding. It has been suggested that small-molecule drugs that elicit the HSR by activating the transcription factor heat shock factor 1 might help mitigate protein misfolding and aggregation in several devastating neurodegenerative disorders, including Huntington disease (HD). In this issue of the JCI, Labbadia et al. use a brain-penetrant Hsp90 inhibitor, HSP990, to induce the HSR in mouse models of HD. Unexpectedly, they observed that HSP990 confers only transient amelioration of a subset of HD-related phenotypes, because alterations in chromatin architecture impair the HSR upon disease progression. These findings suggest that synergistic combination therapies that simultaneously unleash the HSR and prevent its impairment are likely to be needed to restore proteostasis in HD.

摘要

热休克反应 (HSR) 是一种高度保守的保护机制,使细胞能够耐受破坏蛋白质平衡(蛋白质稳态)并促进蛋白质错误折叠的各种环境应激源。有人提出,通过激活热休克因子 1 来引发 HSR 的小分子药物可能有助于减轻几种毁灭性神经退行性疾病(包括亨廷顿病 (HD))中的蛋白质错误折叠和聚集。在本期 JCI 中,Labbadia 等人使用一种脑穿透性 HSP90 抑制剂 HSP990 诱导 HD 小鼠模型中的 HSR。出乎意料的是,他们观察到 HSP990 仅能暂时改善 HD 相关表型的一部分,因为染色质结构的改变会在疾病进展时损害 HSR。这些发现表明,可能需要协同组合疗法来同时引发 HSR 并防止其受损,以恢复 HD 中的蛋白质稳态。