ERp57 modulates mitochondrial calcium uptake through the MCU

Jingquan He; Weikang Shi; Yu Guo; Zhen Chai

doi:10.1016/j.febslet.2014.04.041

ERp57 modulates mitochondrial calcium uptake through the MCU

FEBS Lett. 2014 Jun 5;588(12):2087-94. doi: 10.1016/j.febslet.2014.04.041. Epub 2014 May 8.

Authors

Jingquan He¹, Weikang Shi¹, Yu Guo¹, Zhen Chai²

Affiliations

¹ State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871, China.
² State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871, China. Electronic address: zhenchai@pku.edu.cn.

PMID: 24815697
DOI: 10.1016/j.febslet.2014.04.041

Abstract

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.

Keywords: ERp57; MCU; Mitochondrial calcium uptake.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Base Sequence
Biological Transport
Calcium / metabolism*
Calcium Channels / genetics
Calcium Channels / metabolism*
Gene Expression Regulation
HeLa Cells
Humans
Membrane Potential, Mitochondrial
Mitochondria / metabolism*
Protein Disulfide-Isomerases / deficiency
Protein Disulfide-Isomerases / genetics
Protein Disulfide-Isomerases / metabolism*

Substances

Calcium Channels
mitochondrial calcium uniporter
Protein Disulfide-Isomerases
PDIA3 protein, human
Calcium