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magnesium transporter 1

Der MAGT1 gene provides instructions for making a protein called a magnesium transporter, which moves charged atoms (ions) of magnesium (Mg2+) into certain immune system cells called T cells. T cells recognise foreign invaders, such as viruses, bacteria, and fungi, and are then turned on (activated) to attack these invaders in order to prevent infection and illness. Specifically, the magnesium transporter produced from the MAGT1 gene is active in CD8+ T cells, which are especially important in controlling viral infections such as the Epstein-Barr virus (EBV). These cells normally take in magnesium when they detect a foreign invader, and the magnesium is involved in activating the T cell's response.

Normal function

Der MAGT1 gene provides instructions for making a protein called a magnesium transporter, which moves charged atoms (ions) of magnesium (Mg2+) into certain immune system cells called T cells. T cells recognise foreign invaders, such as viruses, bacteria, and fungi, and are then turned on (activated) to attack these invaders in order to prevent infection and illness. Specifically, the magnesium transporter produced from the MAGT1 gene is active in CD8+ T cells, which are especially important in controlling viral infections such as the Epstein-Barr virus (EBV). These cells normally take in magnesium when they detect a foreign invader, and the magnesium is involved in activating the T cell's response.

Researchers suggest that magnesium transport may also be involved in the production of another type of T cell called helper T cells (CD4+ T cells) in a gland called the thymus. CD4+ T cells direct and assist the functions of the immune system by influencing the activities of other immune system cells.

Conditions referring to this gene or chromosome

Other names

bA217H1.1

DKFZp564K142

IAP

implantation-associated protein

magnesium transporter protein 1

MRX95

oligosaccharyltransferase 3 homolog B

OST3B

PRO0756

XMEN

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  • 18. Aug 2020 | Neueste Version
  • 1 Jun 2014 | Ursprünglich veröffentlicht

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