| 2009 |
MagT1 and TUSC3 function as mammalian plasma membrane Mg2+ transporters: knockdown of either protein significantly lowers total and free intracellular Mg2+ concentrations in mammalian cell lines; MagT1 was identified via yeast complementation screen and its expression is upregulated in low extracellular Mg2+; morpholino knockdown in zebrafish causes early developmental arrest rescued by excess Mg2+ or mammalian mRNA supplementation. |
Yeast complementation screen, siRNA knockdown with intracellular Mg2+ measurement (mag-fura 2), zebrafish morpholino knockdown with rescue experiments |
Proceedings of the National Academy of Sciences of the United States of America |
High |
19717468
|
| 2011 |
MAGT1 mediates a TCR-stimulated Mg2+ flux required for T cell activation; loss of MAGT1 abolishes this flux and attenuates PLCγ1 activation, identifying Mg2+ as a second messenger in the TCR signaling pathway. |
Intracellular Mg2+ flux measurement in T cells from XMEN patients (MAGT1-deficient), PLCγ1 phosphorylation assay, loss-of-function human patient cells |
Magnesium research |
Medium |
21983175
|
| 2011 |
MagT1 overexpression in TRPM7-knockout DT40 B cells augments Mg2+ uptake capacity and rescues growth impairment, demonstrating that MagT1 can partially substitute for TRPM7 as a Mg2+ uptake mechanism; MagT1 expression is upregulated in TRPM7-/- cells. |
Gene expression analysis, overexpression in TRPM7-/- cells with Mg2+ uptake measurement and cell growth assay |
FEBS letters |
Medium |
21627970
|
| 2013 |
Drosophila MagT1 (ortholog of mammalian MAGT1) is a magnesium-selective, non-voltage-dependent channel; its whole-cell currents are upregulated by PKC activation via PMA treatment; PKC-dependent modulation requires Ser100 and Ser108 phosphorylation sites (S100A and S108A mutants abolish PKC-dependent upregulation, while S35A does not). |
Patch-clamp electrophysiology in SH-SY5Y cells expressing wild-type or mutant dMagT1, PKC activator (PMA) treatment with inactive control (4α-PMA), site-directed mutagenesis |
Biochemical and biophysical research communications |
Medium |
23727583
|
| 2018 |
Loss of MAGT1 in mouse B cells impairs Mg2+ homeostasis and increases Ca2+ influx after BCR stimulation, leading to increased phosphorylation of BCR-related proteins with differential effects on PKC activation; Magt1-knockout mice show increased CD19+ and marginal zone B cell frequencies and decreased plasma cell frequencies in spleen. |
Magt1-knockout mouse model, intracellular ion measurement, BCR stimulation assays, flow cytometry, Western blot for phosphoproteins |
Journal of immunology |
High |
29581357
|
| 2018 |
MagT1 is essential for early Drosophila embryonic development; clonal analysis and RNAi knockdown in wing discs show that loss of MagT1 enhances/ectopically activates Wingless (Wnt) signaling and disrupts Decapentaplegic (BMP/TGF-β) signaling; magnesium transport is proportional to MagT1 expression levels in Drosophila S2 cells. |
Drosophila MagT1 mutant generation, clonal analysis, RNAi knockdown, signaling pathway readouts in wing primordia, Mg2+ transport assay in S2 cells |
Biochemical and biophysical research communications |
Medium |
29959918
|
| 2019 |
MAGT1 is the human functional homolog of yeast OST3/OST6 and acts as a subunit of the STT3B oligosaccharyltransferase (OST) complex; MAGT1 deficiency causes selective N-linked glycosylation defects in immune and non-immune glycoproteins including NKG2D and CD28; MAGT1-dependent glycosylation is sensitive to Mg2+ levels; MAGT1 function is partly interchangeable with paralog TUSC3 but they have different tissue distributions. |
MS-based glycoproteomics, CRISPR/Cas9 knockout cell lines, NK cell killing assays, RNA-seq, comparison with TUSC3 |
The Journal of biological chemistry |
High |
31337704
|
| 2019 |
MAGT1 acts as a subunit of the STT3B OST complex mediating N-linked glycosylation; patient cells with MAGT1 mutations show defective post-translational glycosylation of GLUT1 and SHBG (STT3B complex substrates); MAGT1 deficiency is associated with compensatory upregulation of TUSC3. |
Serum transferrin glycosylation analysis in patients, glycosylation substrate analysis (GLUT1, SHBG), patient fibroblast functional studies, protein expression analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
31036665
|
| 2022 |
Reduced steady-state NKG2D (KLRK1) levels in MAGT1-deficient patients are caused by hypoglycosylation of NKG2D protein at a specific site; magnesium supplementation does not rescue NKG2D expression or the hypoglycosylation defect in CRISPR-engineered human cell lines or in an XMEN patient. |
CRISPR-engineered human cell lines, site-specific glycosylation mapping, flow cytometry for NKG2D surface expression, Mg2+ supplementation experiments in cells and patient |
Human genetics |
High |
35182234
|
| 2019 |
MagT1 knockdown in bone marrow mesenchymal stem cells (BMMSCs) reduces intracellular Mg2+, suppresses odontogenic differentiation markers (ALP, DMP-1, DSP), inhibits mineralization, and inactivates the ERK/MAPK signaling pathway; ERK/MAPK pathway activation is required downstream of MagT1-mediated Mg2+ transport for odontogenic differentiation. |
shRNA lentiviral knockdown, intracellular Mg2+ measurement, Western blot for ERK phosphorylation and differentiation markers, flow cytometry, RNA-seq |
Stem cell research & therapy |
Medium |
30704530
|
| 2021 |
MAGT1 knockdown in HeLa cells causes S-phase arrest and apoptosis, reduces ERK1/2 and p38 phosphorylation, increases p21 expression, and alters expression of cell cycle regulators (cyclin-A1, cyclin-B1, MYC, cyclin-D1, cyclin-E1, CDK2); MAGT1 is required for HPV E6/E7-dependent cell cycle progression. |
siRNA knockdown, cell cycle analysis by flow cytometry, Western blot for MAPK phosphorylation and cell cycle proteins, RNA-seq |
Cell cycle |
Medium |
34499581
|
| 2023 |
MAGT1 deficiency in platelets causes defective N-glycosylation of glycoprotein Ibα, glycoprotein VI, and integrin αIIb, leading to impaired platelet aggregation, integrin αIIbβ3 activation, calcium mobilization, PKC activity, and absent PAR1-AP responses; these defects were corrected after hematopoietic stem cell transplantation. |
Platelet function testing (aggregation, calcium flux, integrin activation), N-glycan analysis by mass spectrometry, Western blot for glycoprotein molecular weights, pre/post-HSCT comparison |
Journal of thrombosis and haemostasis |
Medium |
37207862
|
| 2023 |
MAGT1-deficient mice show accelerated arterial thrombosis, shortened bleeding time, and increased GPVI-dependent platelet aggregation due to increased Ca2+ influx and hyperphosphorylation of Syk, LAT, and PLCγ2; the inhibitory PKC loop is impaired; MgCl2 supplementation or TRPC6 channel blockade normalizes aggregation; haploinsufficiency of TRPC6 in Magt1-/- mice normalizes GPVI signaling and thrombus formation in vivo, establishing functional linkage between MAGT1 and TRPC6. |
Magt1-knockout mouse model, in vivo arterial thrombosis models, transient MCAO stroke model, platelet signaling (phospho-Western blot), Ca2+ flux measurement, pharmacological inhibition, TRPC6/Magt1 double-mutant mice, human XMEN patient platelet validation |
Arteriosclerosis, thrombosis, and vascular biology |
High |
37381987
|
| 2008 |
MagT1 protein is expressed in rumen epithelial cells and functions as a Mg2+ influx transporter; its protein abundance is regulated by extracellular Mg2+ concentration (decreased by low Mg2+, increased by high Mg2+); functional Mg2+ transport capacity is correspondingly altered. |
RT-PCR, Western blot, flow cytometry, immunocytochemistry, intracellular Mg2+ measurement with mag-fura 2 |
Magnesium research |
Medium |
18705540
|
| 2024 |
MagT1 mediates Mg2+ uptake required for N-linked glycosylation of SPARC (secreted protein acidic and rich in cysteine); SPARC glycosylation affects its extracellular secretion and mineral deposition; established using RNAi knockdown and glycosylation inhibitors in the context of magnesium-impregnated membrane-driven osteogenesis. |
RNAi knockdown, glycosylation inhibitors, immunostaining, DDC-SEM for mineral deposition, in vivo rat skull defect model |
Advanced healthcare materials |
Medium |
39632347
|
| 2017 |
miR-199a-5p directly targets MAGT1 mRNA and suppresses its expression post-transcriptionally, validated by luciferase reporter assay; this mechanism contributes to reduced MAGT1 protein (without mRNA change) and functional depletion of CD8+ T cells in chronic HBV infection. |
Luciferase reporter assay, lentiviral overexpression/knockdown of miR-199a-5p, qRT-PCR for mRNA, Western blot for protein, immune function assays |
Scientific reports / Magnesium research |
Medium |
29051561 31038761 33210605
|