The mechanism of αB-crystallin gene expression by proteasome inhibition
The mechanism of αB-crystallin gene expression by proteasome inhibition
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DOI：
10.1016/j.bbrc.2003.09.186
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发表时间：
2003-11-07
影响因子：
3.1
通讯作者：
Mizukami, Y
中科院分区：
文献类型：
--
作者：
Aki, T;Yoshida, K;Mizukami, Y
研究了蛋白酶体抑制小热休克蛋白/ α -结晶蛋白基因表达的机制。蛋白酶体抑制和热休克均能有效诱导α -结晶蛋白的表达，而热休克和蛋白酶体抑制均能有效诱导HSP27的表达。alphaB-crystallin基因的启动子包含两个保守的热休克元件，一个位于-397和-374之间，另一个位于-57和-37之间，相对于转录起始位点。电泳迁移迁移试验（EMSA）显示，蛋白酶体抑制诱导热休克因子与α -结晶蛋白基因启动子中的热休克元件结合。然而，使用缺失构建的瞬时转染实验表明，-373和-58之间的区域在启动子活性中起重要作用。这些结果表明，α -结晶蛋白基因表达对蛋白酶体抑制和热休克的响应机制存在差异，热休克元件的激活不足以使α -结晶蛋白基因被蛋白酶体抑制有效诱导。(C) 2003 Elsevier Inc.版权所有。
The mechanism of small heat shock protein/alphaB-crystallin gene expression by proteasome inhibition was investigated. Expression of alphaB-crystallin was induced efficiently only by proteasome inhibition and not by heat shock while expression of HSP27 was induced efficiently by both proteasome inhibition and heat shock. The promoter of the alphaB-crystallin gene contains two conserved heat shock elements, one located between -397 and -374 and the other between -57 and -37, relative to the transcription start site. Electrophoretic mobility shift assay (EMSA) revealed that proteasome inhibition induces binding of heat shock factors to both heat shock elements in the alphaB-crystallin gene promoter. However, a transient transfection assay using deletion constructs of the alphaB-crystallin gene promoter showed that the region between -373 and -58 plays an important role in promoter activity. These results indicate the presence of differential response mechanisms of alphaB-crystallin gene expression to proteasome inhibition and heat shock, and that the activation of heat shock elements is not sufficient for the efficient induction of the alphaB-crystallin gene by proteasome inhibition. (C) 2003 Elsevier Inc. All rights reserved.