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FEBS Lett. 2011 Jul 21;585(14):2275-8. doi: 10.1016/j.febslet.2011.05.052. Epub 2011 May 27.

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

Author information

1
Integrated Department of Immunology, National Jewish Health and University of Colorado, Denver, CO 80206, USA.

Abstract

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+).

PMID:
21627970
PMCID:
PMC3139019
DOI:
10.1016/j.febslet.2011.05.052
[Indexed for MEDLINE]
Free PMC Article

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