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    Solute carrier 41A3 encodes for a mitochondrial Mg(2+) efflux system (2016)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Mastrototaro, Lucia (WE 2)
    Smorodchenko, Alina
    Aschenbach, Jörg R (WE 2)
    Kolisek, Martin (WE 2)
    Sponder, Gerhard (WE 2)
    Quelle
    Scientific reports; 6(27999) — S. 1–14
    ISSN: 2045-2322
    Sprache
    Englisch
    Verweise
    URL (Volltext): http://www.nature.com/articles/srep27999
    DOI: 10.1038/srep27999
    Pubmed: 27302215
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    Institut für Veterinär-Physiologie

    Oertzenweg 19 b
    14163 Berlin
    Tel.+49 30 838 62600 Fax.+49 30 838-62610
    email:physiologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    The important role of magnesium (Mg(2+)) in normal cellular physiology requires flexible, yet tightly regulated, intracellular Mg(2+) homeostasis (IMH). However, only little is known about Mg(2+) transporters of subcellular compartments such as mitochondria, despite their obvious importance for the deposition and reposition of intracellular Mg(2+) pools. In particular, knowledge about mechanisms responsible for extrusion of Mg(2+) from mitochondria is lacking. Based on circumstantial evidence, two possible mechanisms of Mg(2+) release from mitochondria were predicted: (1) Mg(2+) efflux coupled to ATP translocation via the ATP-Mg/Pi carrier, and (2) Mg(2+) efflux via a H(+)/Mg(2+) exchanger. Regardless, the identity of the H(+)-coupled Mg(2+) efflux system is unknown. We demonstrate here that member A3 of solute carrier (SLC) family 41 is a mitochondrial Mg(2+) efflux system. Mitochondria of HEK293 cells overexpressing SLC41A3 exhibit a 60% increase in the extrusion of Mg(2+) compared with control cells. This efflux mechanism is Na(+)-dependent and temperature sensitive. Our data identify SLC41A3 as the first mammalian mitochondrial Mg(2+) efflux system, which greatly enhances our understanding of intracellular Mg(2+) homeostasis.