The Mg<sup>2+</sup>
 transporter MagT1 partially rescues cell growth and Mg<sup>2+</sup>
 uptake in cells lacking the channel-kinase TRPM7

Deason-Towne, Francina; Perraud, Anne‐Laure; Schmitz, C.

doi:10.1016/j.febslet.2011.05.052

Cited by 58 publications

(58 citation statements)

References 20 publications

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“…Previous studies have suggested that the melastatin subfamily 6 and 7 of the transient receptor potential cation channels (TRPM6 and TRPM7) and MagT1 are implicated in Mg 2+ influx [37]. Na + /Mg 2+ exchanger, which was shown to be the predominant route (about 97%) for [Mg 2+ ] i efflux, is associated with [Mg 2+ ] i homeostasis in mammalian cells [15].…”

Section: Discussionmentioning

confidence: 99%

“…Over the past decades, a number of magnesium transporters and transport pathways have been demonstrated to keep cellular Mg 2+ homeostasis, such as TRPM6, TRPM7, MagT1, Na + /Mg 2+ exchanger, SLC41A1 and SLC41A2 [37,16,17]. Previous studies have suggested that the melastatin subfamily 6 and 7 of the transient receptor potential cation channels (TRPM6 and TRPM7) and MagT1 are implicated in Mg 2+ influx [37].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

SLC41A1 knockdown inhibits angiotensin II-induced cardiac fibrosis by preventing Mg2+ efflux and Ca2+ signaling in cardiac fibroblasts

Jiang

et al. 2014

Archives of Biochemistry and Biophysics

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

SLC41A1 knockdown inhibits angiotensin II-induced cardiac fibrosis by preventing Mg2+ efflux and Ca2+ signaling in cardiac fibroblasts

Jiang

et al. 2014

Archives of Biochemistry and Biophysics

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“…In analogy, TRPM7 deficient chicken DT40 B-cells go into cell-growth arrest and die under physiological levels of Mg 2+ (~1mM), but grow normally if the medium is supplemented with 5-10 mM Mg 2+ . TRPM7 -/- DT40 cells can be rescued by overexpression of human TRPM7 WT, TRPM7 kinase dead mutants [10], and partially by the human Mg 2+ transporters MagT1 [30] and SLC41A2 [31], but not via overexpression of TRPM6 WT alone [11]. …”

Section: Introductionmentioning

confidence: 99%

TRPM6 kinase activity regulates TRPM7 trafficking and inhibits cellular growth under hypomagnesic conditions

Brandao

Deason-Towne

Zhao

et al. 2014

Cell. Mol. Life Sci.

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The channel kinases TRPM6 and TRPM7 are both members of the melastatin related transient receptor potential (TRPM) subfamily of ion channels and the only known fusions of an ion channel pore with a kinase domain. TRPM6 and TRPM7 form functional, tetrameric channel complexes at the plasma membrane by heteromerization. TRPM6 was previously shown to cross-phosphorylate TRPM7 on threonine residues, but not vice versa. Genetic studies demonstrated that TRPM6 and TRPM7 fulfill non-redundant functions, and that each channel contributes uniquely to the regulation of Mg2+ homeostasis. Although there are indications that TRPM6 and TRPM7 can influence each other’s cellular distribution and activity, little is known about the functional relationship between these two channel-kinases. In the present study, we examined how TRPM6 kinase activity influences TRPM7 serine phosphorylation, intracellular trafficking, and cell surface expression of TRPM7, as well as Mg2+-dependent cellular growth. We found TRPM7 serine phosphorylation via the TRPM6 kinase, but no TRPM6 serine phosphorylation via the TRPM7 kinase. Intracellular trafficking of TRPM7 was altered in HEK-293 epithelial kidney cells and DT40 B cells in the presence of TRPM6 with intact kinase activity, independently of the availability of extracellular Mg2+, but TRPM6/7 surface labeling experiments indicate comparable levels of the TRPM6/7 channels at the plasma membrane. Furthermore, using a complementation approach in TRPM7-deficient DT40 B-cells, we demonstrated that wildtype TRPM6 inhibited cell growth under hypomagnesic cell culture conditions in cells co-expressing TRPM6 and TRPM7, however co-expression of a TRPM6 kinase dead mutant had no effect – a similar phenotype was also observed in TRPM6/7 co-expressing HEK-293 cells. Our results provide first clues about how heteromer formation between TRPM6 and TRPM7 influences the biological activity of these ion channels. We show that TRPM6 regulates TRPM7 intracellular trafficking and TRPM7 dependent cell growth. All these effects are dependent upon the presence of an active TRPM6 kinase domain. Dysregulated Mg2+-homeostasis causes or exacerbates many pathologies. As TRPM6 and TRPM7 are expressed simultaneously in numerous cell types, understanding how their relationship impacts regulation of Mg2+-uptake is thus important knowledge.

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“…The controlled overexpression of transfected MagT1 in DT40 B lymphocytes partially rescues the growth and the maintenance of intracellular levels of Mg 2? in the absence of the ion channel TRPM7 [35]. Thus, MagT1 appears to play an important role in the regulation of intracellular Mg 2?…”

Section: Magt1 Is a Plasma Membrane Mg 21 Transportermentioning

confidence: 97%

The role of Mg2+ in immune cells

et al. 2012

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The physiological and clinical relevance of Mg(2+) has evolved over the last decades. The molecular identification of multiple Mg(2+) transporters (Acdp2, MagT1, Mrs2, Paracellin-1, SLC41A1, SLC41A2, TRPM6 and TRPM7) and their biophysical characterization in recent years has improved our understanding of Mg(2+) homeostasis regulation and has provided a basis for investigating the role of Mg(2+) in the immune system. Deletions and mutations of Mg(2+) transporters produce severe phenotypes with more systemic symptoms than those seen with Ca(2+) channel deletions, which tend to be more specific and less profound. Deficiency of the Mg(2+) permeable ion channels TRPM6 or TRPM7 in mice is lethal at embryonic day 12.5 or at day 6.5, respectively, and, even more surprisingly, chicken DT40 B cells lacking TRPM7 die after 24-48 h. Recent progress made in Mg(2+) research has helped to define underlying mechanisms of two hereditary diseases, human Hypomagnesemia (TRPM6 deletion) and X-chromosomal immunodeficiency (MagT1 deletion), and has revealed a potential new role for Mg(2+) as a second messenger. Future elucidation of human Mg(2+) transporters (Mrs2, SLC41A1, SLC41A2, TRPM7) expressed in immunocytes, beyond MagT1 and TRPM6, will widen our knowledge about the potential role of Mg(2+) in the activation of the immune response.

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

Cited by 58 publications

References 20 publications

SLC41A1 knockdown inhibits angiotensin II-induced cardiac fibrosis by preventing Mg2+ efflux and Ca2+ signaling in cardiac fibroblasts

SLC41A1 knockdown inhibits angiotensin II-induced cardiac fibrosis by preventing Mg2+ efflux and Ca2+ signaling in cardiac fibroblasts

TRPM6 kinase activity regulates TRPM7 trafficking and inhibits cellular growth under hypomagnesic conditions

The role of Mg2+ in immune cells

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

Cited by 58 publications

References 20 publications

SLC41A1 knockdown inhibits angiotensin II-induced cardiac fibrosis by preventing Mg2+ efflux and Ca2+ signaling in cardiac fibroblasts

SLC41A1 knockdown inhibits angiotensin II-induced cardiac fibrosis by preventing Mg2+ efflux and Ca2+ signaling in cardiac fibroblasts

TRPM6 kinase activity regulates TRPM7 trafficking and inhibits cellular growth under hypomagnesic conditions

The role of Mg2+ in immune cells

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