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 Printable version |
Molecular components of vertebrate Mg
2+-homeostasis regulation |
Magnesium Research. Volume 20, Number 1, 6-18, March 2007, Review article
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 Free Article
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Author(s) : Carsten Schmitz, Francina Deason, Anne-Laure Perraud |
Summary : Over the past decades, the clinical relevance and biological significance of Mg
2+ have been thoroughly documented. Although multiple Mg
2+-transport pathways have been biophysically characterized, the molecular identity of the postulated components of Mg
2+-homeostasis regulation in vertebrates remain undefined. Recent advances in the fields of genetics, genomics and proteomics, and novel technologies such as cDNA microarrays have allowed for substantial progress in this area. The mitochondrial Mrs2 protein was the first human Mg
2+ transporter characterized as such, and an important element for future analyses of the role of mitochondria in managing intracellular Mg
2+. Several molecules with Mg
2+-transport capabilities have been identified through a screen designed to find genes upregulated under hypomagnesic conditions. This includes SLC41A1 and 2, ACDP2 and MagT1. Finally, the elucidation of the molecular cause underlying two different hereditary diseases leading to hypomagnesemia resulted in the cloning and characterization of claudin 16 (paracellin-1), and TRPM6. Whereas claudin 16 plays a crucial role in paracellular Mg
2+ transport, TRPM6 is involved in the transcellular pathway. TRPM6 and its closest relative TRPM7 are both puzzling ion channel-kinase fusions, and perhaps the most unexpected newly identified players in the regulation of Mg
2+-homeostasis in vertebrates. |
Keywords : Mrs2, ACDP2, SLC41A1 and 2, Paracellin-1, Claudin 16, MagT1, TRPM6, TRPM7 |
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