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The Mg 2+ transporter MagT1 partially rescues cell growth and Mg 2+ uptake in cells lacking the channel‐kinase TRPM7
Author(s) -
Deason-Towne Francina,
Perraud Anne-Laure,
Schmitz Carsten
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.05.052
Subject(s) - trpm7 , cytosol , extracellular , homeostasis , transporter , microbiology and biotechnology , downregulation and upregulation , kinase , cell growth , chemistry , intracellular , biology , biophysics , biochemistry , ion channel , gene , enzyme , receptor
Magnesium (Mg 2+ ) transport across membranes plays an essential role in cellular growth and survival. TRPM7 is the unique fusion of a Mg 2+ permeable pore with an active cytosolic kinase domain, and is considered a master regulator of cellular Mg 2+ homeostasis. We previously found that the genetic deletion of TRPM7 in DT40 B cells results in Mg 2+ deficiency and severe growth impairment, which can be rescued by supplementation with excess extracellular Mg 2+ . Here, we show that gene expression of the Mg 2+ selective transporter MagT1 is upregulated in TRPM7 −/− cells. Furthermore, overexpression of MagT1 in TRPM7 −/− cells augments their capacity to uptake Mg 2+ , and improves their growth behavior in the absence of excess Mg 2+ .