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内质网中折叠容量的调节增加可防止未折叠蛋白应激。

Regulated increase in folding capacity prevents unfolded protein stress in the ER.

机构信息

Cellular Protein Chemistry, Bijvoet Center for Biomolecular Research, Utrecht University, The Netherlands.

出版信息

J Cell Sci. 2010 Mar 1;123(Pt 5):787-94. doi: 10.1242/jcs.041111. Epub 2010 Feb 9.

DOI:10.1242/jcs.041111
PMID:20144991
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2823579/
Abstract

Stimulation of thyrocytes with thyroid stimulating hormone (TSH) leads to a morphological change and a massive increase in thyroglobulin (Tg) production. Although Tg is a demanding client of the endoplasmic reticulum (ER), its increase did not result in significant accumulation of unfolded protein in the ER. Instead, ER chaperones and folding enzymes reached maximum synthesis rates immediately after TSH stimulation, before significant upregulation of Tg synthesis. The resulting increase in folding capacity before client protein production prevented cellular unfolded-protein stress, confirmed by the silence of the most conserved branch of the unfolded protein response. Thyrocytes set an example of physiological adaptation of cells to a future potentially stress-causing situation, which suggests a general strategy for both non-secretory and specialized secretory cells.

摘要

促甲状腺激素(TSH)刺激甲状腺细胞会导致形态变化和甲状腺球蛋白(Tg)产量的大量增加。尽管 Tg 是内质网(ER)的一个要求苛刻的客户,但它的增加并没有导致 ER 中未折叠蛋白的大量积累。相反,ER 伴侣蛋白和折叠酶在 TSH 刺激后立即达到最大合成速率,然后 Tg 合成才显著上调。在产生客户蛋白之前,折叠能力的增加导致细胞未折叠蛋白应激,这一现象被未折叠蛋白反应中最保守分支的沉默所证实。甲状腺细胞为细胞对未来潜在应激情况的生理适应树立了榜样,这为非分泌细胞和专门分泌细胞提供了一种普遍的策略。

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本文引用的文献

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XBP-1 regulates signal transduction, transcription factors and bone marrow colonization in B cells.XBP-1调节B细胞中的信号转导、转录因子和骨髓定植。
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