The Mg2+ transporter MagT1 partially rescues cell growth and Mg2+ uptake in cells lacking the channel-kinase TRPM7
The Mg2+ transporter MagT1 partially rescues cell growth and Mg2+ uptake in cells lacking the channel-kinase TRPM7
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DOI：
10.1016/j.febslet.2011.05.052
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发表时间：
2011-07-21
期刊：
影响因子：
3.5
通讯作者：
Schmitz, Carsten
中科院分区：
文献类型：
--
作者：
Deason-Towne, Francina;Perraud, Anne-Laure;Schmitz, Carsten
镁 (Mg2+) 跨膜运输在细胞生长和存活中发挥着重要作用。 TRPM7 是 Mg2+ 渗透孔与活性胞质激酶结构域的独特融合，被认为是细胞 Mg2+ 稳态的主要调节因子。我们之前发现DT40 B细胞中TRPM7的基因缺失会导致Mg2+缺乏和严重的生长障碍，可以通过补充过量的细胞外Mg2+来挽救。在这里，我们发现 TRPM7(-/-) 细胞中 Mg2+ 选择性转运蛋白 MagT1 的基因表达上调。此外，TRPM7(-/-)细胞中MagT1的过度表达增强了它们摄取Mg2+的能力，并改善了它们在没有过量Mg2+的情况下的生长行为。 (C) 2011 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
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.