The Mg2+ transporter MagT1 partially rescues cell growth and Mg2+ uptake in cells lacking the channel-kinase TRPM7

被引:51
作者
Deason-Towne, Francina
Perraud, Anne-Laure [1 ]
Schmitz, Carsten
机构
[1] Natl Jewish Hlth, Integrated Dept Immunol, Denver, CO 80206 USA
基金
美国国家卫生研究院;
关键词
MagT1; Mg2+ homeostasis; Channel-kinase; TRPM7; complementation; DT40 B cell; RUMEN EPITHELIAL-CELLS; SECONDARY HYPOCALCEMIA; EMBRYONIC-DEVELOPMENT; MAGNESIUM; HOMEOSTASIS; IDENTIFICATION; HYPOMAGNESEMIA;
D O I
10.1016/j.febslet.2011.05.052
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Magnesium (Mg2+) transport across membranes plays an essential role in cellular growth and survival. TRPM7 is the unique fusion of a Mg2+ permeable pore with an active cytosolic kinase domain, and is considered a master regulator of cellular Mg2+ homeostasis. We previously found that the genetic deletion of TRPM7 in DT40 B cells results in Mg2+ deficiency and severe growth impairment, which can be rescued by supplementation with excess extracellular Mg2+. Here, we show that gene expression of the Mg2+ selective transporter MagT1 is upregulated in TRPM7(-/-) cells. Furthermore, overexpression of MagT1 in TRPM7(-/-) cells augments their capacity to uptake Mg2+, and improves their growth behavior in the absence of excess Mg2+. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:2275 / 2278
页数:4
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