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Magnesium transporter 1 (MAGT1)

Target
MAGT1
Molecular classification
Transporter (specifically, magnesium ion transporter), Component of the oligosaccharyltransferase complex (glycosyltransferase), Sometimes grouped with Solute carrier proteins (SLC family), SLC58A1
01

Overview

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].

Other names
Magnesium transporter 1MAGT1Dolichyl-diphosphooligosaccharide--protein glycosyltransferase subunit MAGT1Oligosaccharyl transferase subunit MAGT1Implantation-associated proteinSLC58A1OST3BMRX95XMENIAPMagT1IAG2CDG1CColigosaccharyltransferase 3 homolog BbA217H1.1DKFZp564K142PSEC0084UNQ628/PRO1244PRO0756
02

Mechanism of action

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.

03

Biological functions

Magnesium ion transport (influx and homeostasis)N-glycosylation of proteins (as part of N-oligosaccharyltransferase complex)Immune responses (especially activation of CD8+ and CD4+ T cells)Cell proliferation, differentiation, and oncogenic transformationRegulation of T cell receptor activation and NK cell function
04

Disease associations

Immunodeficiency (e.g., XMEN syndrome: X-linked immunodeficiency with magnesium defect, Epstein-Barr virus infection, and neoplasia)Cancer (e.g., lymphoma association via EBV infection, hepatocellular carcinoma)Intellectual disability (X-linked forms)Congenital disorder of glycosylation (Type Icc)Autoimmune lymphoproliferative syndromeOther features: neurodevelopmental disorders, abnormal skin phenotypes
05

Safety considerations

Risk of immunodeficiency and increased susceptibility to EBV-associated cancer if MAGT1 is dysfunctional or antagonizedOff-target effects on glycosylation pathways when modulating MAGT1 or its associated OST complexImpact on systemic magnesium balance and related metabolic complicationsGene therapy approaches present general gene editing risks (immune reactions, insertional mutagenesis)
06

Interacting drugs

No approved drugs directly target MAGT1 at present based on available literature and drug databases

2 more in the full profile.

07

Biomarkers

MAGT1 gene mutation (for XMEN syndrome diagnosis)Intracellular magnesium levels in T cellsT cell activation markers in the presence of MAGT1 dysfunction

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