Vanadate inhibits endoplasmic reticulum stress responses
Vanadate inhibits endoplasmic reticulum stress responses
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DOI：
10.1016/j.ejphar.2008.07.034
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发表时间：
2008-10-10
影响因子：
5
通讯作者：
Ozawa, Koichiro
中科院分区：
文献类型：
--
作者：
Hosoi, Toru;Saito, Atsushi;Ozawa, Koichiro
内质网功能的破坏导致未折叠蛋白质的积累，这导致内质网应激。在本研究中，我们研究了钒酸盐对这种应力的影响。内质网应激增加了神经胶质细胞培养物中葡萄糖调节蛋白78（GRP 78）和CCAAT/增强子结合蛋白同源蛋白（CHOP）的表达。我们发现，钒酸盐抑制内质网应激引起的GRP 78和CHOP表达的增加在mRNA和蛋白水平。因此，这些结果表明，钒酸调节内质网应激反应和新的钒酸响应蛋白可能参与这些过程。皇冠版权所有2008年出版的爱思唯尔B. V.保留所有权利。
The disruption of endoplasmic reticulum function leads to an accumulation of unfolded proteins, which results in endoplasmic reticulum stress. In the present study, we investigated the effect of vanadate on such stress. Endoplasmic reticulum stress increased glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP) expressions in glial cell cultures. We found that vanadate inhibited the endoplasmic reticulum stress-induced increase in GRP78 and CHOP expressions at both mRNA and protein levels. Thus, these results suggest that vanadate modulates endoplasmic reticulum stress responses and that novel vanadate-responsive protein(s) might be involved in these processes. Crown Copyright 2008 Published by Elsevier B.V. All rights reserved.