ERp57 modulates mitochondrial calcium uptake through the MCU
ERp57 modulates mitochondrial calcium uptake through the MCU
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ERp57 通过 MCU 调节线粒体钙摄取
DOI：
10.1016/j.febslet.2014.04.041
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发表时间：
2014-06-05
期刊：
影响因子：
3.5
通讯作者：
Chai, Zhen
中科院分区：
文献类型：
--
作者：
He, Jingquan;Shi, Weikang;Chai, Zhen
ERp57 参与钙稳态的调节。尽管 ERp57 调节跨质膜和内质网膜的钙通量，但其在线粒体上的功能很大程度上未知。在这里，我们发现ERp57可以调节线粒体钙单向转运蛋白（MCU）的表达并调节线粒体钙的摄取。在 ERp57 沉默的 HeLa 细胞中，MCU 下调，线粒体钙摄取受到抑制，与 MCU 敲低的效果一致。当 MCU 在 ERp57 敲低细胞中重新表达时，线粒体钙摄取恢复。因此，ERp57 是线粒体钙稳态的有效调节剂。 (C) 2014 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
ERp57 participates in the regulation of calcium homeostasis. Although ERp57 modulates calcium flux across the plasma membrane and the endoplasmic reticulum membrane, its functions on mitochondria are largely unknown. Here, we found that ERp57 can regulate the expression of the mitochondrial calcium uniporter (MCU) and modulate mitochondrial calcium uptake. In ERp57-silenced HeLa cells, MCU was downregulated, and the mitochondrial calcium uptake was inhibited, consistent with the effect of MCU knockdown. When MCU was re-expressed in the ERp57 knockdown cells, mitochondrial calcium uptake was restored. Thus, ERp57 is a potent regulator of mitochondrial calcium homeostasis. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.