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Magnesium transporter 1 (MAGT1) is a ubiquitously expressed plasma membrane protein responsible for maintaining cellular magnesium homeostasis by facilitating the influx of Mg\(^{2+}\) ions[1][2][3][4]. MAGT1 is especially important in T cells, where its magnesium transport activity is essential for T cell receptor signaling and effective immune responses, notably against viral infections such as Epstein-Barr virus (EBV)[2]. Aside from ion transport, MAGT1 serves as an accessory component of the oligosaccharyltransferase (OST) complex, participating in the N-glycosylation of specific proteins, particularly those relevant for immune cell function[3]. Mutations or dysfunctions in MAGT1 underlie human diseases including XMEN syndrome—characterized by immunodeficiency, chronic EBV infection, and increased risk of lymphoma—as well as X-linked intellectual disability and congenital disorders of glycosylation[2][3][1]. MAGT1’s role in magnesium homeostasis, glycosylation, and immune regulation makes it a therapeutic target of interest for genetic and immunological intervention, though targeted pharmacological agents are not currently available[1][2][3][4].
Gene therapy: correction of MAGT1 loss-of-function mutations to restore normal T cell activation. Magnesium supplementation: restoration of intracellular magnesium to attempt compensation for defective transport.
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