Affinage

MGAT3

Beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase · UniProt Q09327

Length
533 aa
Mass
61.3 kDa
Annotated
2026-06-10
36 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MGAT3 encodes GlcNAc-TIII (GnT-III), a Golgi-resident type II transmembrane glycosyltransferase that transfers N-acetylglucosamine in β1,4 linkage to the β-linked mannose of the trimannosyl N-glycan core to produce a bisecting GlcNAc residue that suppresses further N-glycan branching (PMID:8370666, PMID:7590346). Catalysis depends on conserved acidic active-site residues—Glu320 as the catalytic center and Asp321/Asp323—mutation of which abolishes activity, with a catalytically dead Asp323 mutant acting dominant-negatively to block bisected-glycan formation (PMID:11784313, PMID:38936637); an internal loop suppresses catalytic activity and harbors the shedding cleavage site, while a C-terminal tail is required for proper folding and Golgi retention, with its loss causing ER mislocalization and accelerated degradation (PMID:39653250). Despite this molecular activity, bisecting GlcNAc is dispensable for normal mouse development, as Mgat3-null mice are viable and fertile (PMID:9061364). GnT-III modifies a defined set of glycoprotein substrates—including CD45, E-cadherin, ICAM-1, haptoglobin, CD82 at Asn157, and α-galactosidase A (GLA)—and these modifications carry distinct functional consequences: bisecting glycosylation of E-cadherin and ICAM-1 restrains EMT and cell adhesion/migration (PMID:22427986, PMID:23300837), glycosylation of CD82 disrupts integrin α5β1-mediated adhesion to fibronectin to inhibit ovarian cancer migration and metastasis (PMID:32483464), control of Notch receptor trafficking redirects the receptor to the lysosome to limit cancer stem-cell expansion (PMID:28842505), and bisecting GlcNAc on GLA promotes its degradation to inhibit breast cancer progression (PMID:39851531). MGAT3 expression is controlled epigenetically by promoter/transcription-start-site methylation and transcriptionally through Wnt/β-catenin and Akt/GSK-3β signaling, as well as post-transcriptionally by miR-23b targeting of its 3′-UTR (PMID:22427986, PMID:24619415, PMID:27429195, PMID:29223528, PMID:34153312).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1993 High

    Establishing what MGAT3 is at the molecular level: cloning revealed it encodes a type II transmembrane glycosyltransferase that builds the bisecting GlcNAc on the N-glycan core.

    Evidence cDNA cloning, ORF analysis, and FISH mapping of human GnT-III

    PMID:8370666

    Open questions at the time
    • Did not resolve active-site residues or catalytic mechanism
    • Substrate glycoproteins not yet identified
  2. 1995 High

    Confirmed the cloned ORF is the catalytic enzyme and not a regulatory factor by demonstrating that sense-orientation expression confers GlcNAc-TIII activity.

    Evidence Genomic cloning and sense/antisense transfection with enzymatic assay in CHO cells

    PMID:7590346

    Open questions at the time
    • Tissue-restricted expression mechanism unexplained
    • No physiological substrate defined
  3. 1995 Medium

    Linked elevated GnT-III activity in hematologic malignancy to a concrete physiological substrate, identifying CD45 as bearing increased bisecting GlcNAc.

    Evidence Enzymatic assay, immunoprecipitation, and E4-PHA lectin blot in CML/myeloma cells

    PMID:7829256

    Open questions at the time
    • Functional consequence of CD45 bisecting glycosylation not established
    • Single-lab characterization
  4. 1997 High

    Resolved whether bisecting GlcNAc is essential in vivo: knockout mice showed it is dispensable for development and homeostasis, redirecting the field toward conditional/disease roles.

    Evidence Cre/loxP gene targeting with lectin, flow, and histology readouts

    PMID:9061364

    Open questions at the time
    • Phenotypes under stress, tumor, or aging not assessed
    • Compensation by other branching enzymes not excluded
  5. 2002 High

    Defined the catalytic chemistry by mapping required active-site aspartates and demonstrating dominant-negative suppression by an inactive mutant.

    Evidence Homology-guided site-directed mutagenesis with activity and N-glycan structural analysis

    PMID:11784313

    Open questions at the time
    • Did not identify the principal catalytic residue (later Glu320)
    • No structural model of the active site
  6. 2002 Medium

    Connected GnT-III to tumor suppression in vivo and expanded the substrate repertoire by identifying haptoglobin as a bisected target.

    Evidence GnT-III transgenic DEN-hepatocarcinogenesis model with glycomic/immunoprecipitation substrate mapping

    PMID:12420740

    Open questions at the time
    • Mechanism linking haptoglobin glycosylation to tumor suppression unclear
    • Single-lab study
  7. 2012 Medium

    Showed how MGAT3 is regulated and coupled to cell-state transitions: promoter methylation silences it during EMT and is reversed in MET, controlling E-cadherin glycosylation.

    Evidence Bisulfite sequencing and lectin/glycan analysis during TGF-β-induced EMT/MET

    PMID:22427986

    Open questions at the time
    • Upstream signals driving methylation not defined
    • Causality of E-cadherin glycosylation in EMT not proven by rescue
  8. 2012 Medium

    Identified an inducible transcriptional route (ATRA/ERK) to GnT-III upregulation and tied ICAM-1 glycan remodeling to suppressed adhesion and transmigration.

    Evidence siRNA, gel mobility/PNGase F, adhesion and trans-endothelial migration assays with ERK inhibition

    PMID:23300837

    Open questions at the time
    • Direct transcriptional effectors downstream of ERK not mapped
    • Single-lab characterization
  9. 2014 Medium

    Placed MGAT3 in a glycan crosstalk network: loss of core fucose induces GnT-III via Wnt/β-catenin, increasing bisecting GlcNAc on integrin and N-cadherin.

    Evidence Fut8-/- MEFs with Wnt-inhibitor epistasis and in vivo IgG mass spectrometry

    PMID:24619415

    Open questions at the time
    • How loss of core fucose activates Wnt signaling not resolved
    • Single-lab study
  10. 2016 Medium

    Generalized methylation control of MGAT3 to cancer, directly tying promoter demethylation to restored bisecting-glycan biosynthesis.

    Evidence 5-Aza treatment, bisulfite sequencing, and LC-MS/MS glycan detection in ovarian cancer cells

    PMID:27429195

    Open questions at the time
    • Functional impact of restored MGAT3 in this model not measured
    • Single-lab study
  11. 2017 Medium

    Uncovered a trafficking-based mechanism for MGAT3's tumor-relevant role: bisecting glycosylation controls Notch receptor lysosomal routing to limit cancer stem-cell expansion.

    Evidence shRNA knockdown, side-population flow cytometry, lysosomal localization, and γ-secretase comparison in ovarian carcinoma cells

    PMID:28842505

    Open questions at the time
    • Direct demonstration that Notch itself is bisected not shown
    • Single-lab study
  12. 2017 Medium

    Established an Akt/GSK-3β/β-catenin signaling axis as upstream regulator of GnT-III in a neurodegeneration context.

    Evidence APP/PS1 mice and Aβ-treated PC12 cells with β-catenin siRNA and PI3K inhibitor epistasis

    PMID:29223528

    Open questions at the time
    • Direct substrate(s) mediating neural effects not identified
    • Single-lab study
  13. 2020 High

    Provided rigorous site-resolved substrate causality: MGAT3 glycosylation of CD82 at Asn157 is required to suppress integrin α5β1/fibronectin adhesion and metastasis.

    Evidence CD82 glycosite mutagenesis with in vitro/in vivo migration, adhesion assays, and paired tissues

    PMID:32483464

    Open questions at the time
    • Structural basis of how the bisected glycan alters CD82-integrin interaction not defined
    • Single-lab study
  14. 2021 Medium

    Added post-transcriptional control by showing miR-23b directly targets the GnT-III 3′-UTR, with downstream effects on tau phosphorylation and oxidative stress.

    Evidence Dual-luciferase 3′-UTR reporter and overexpression in Aβ-induced AD models

    PMID:34153312

    Open questions at the time
    • Whether GnT-III substrate changes mediate the tau/oxidative effects not shown
    • Single-lab study
  15. 2024 Medium

    Resolved the catalytic center and a localization-dependent activity mechanism: Glu320 is catalytic, and a K346T mutant shifts to the cis-Golgi to explain discordant in vitro vs intracellular activity.

    Evidence AlphaFold2 modeling, mutagenesis, in vitro/intracellular activity, TurboID localization, and cycloheximide chase

    PMID:38936637

    Open questions at the time
    • No experimental crystal/cryo-EM structure
    • Single-lab study
  16. 2024 Medium

    Dissected domain-level regulation: an internal loop autoinhibits and is the shedding cleavage site, while the C-terminal tail is needed for folding and Golgi retention.

    Evidence Deletion mutagenesis with activity assays and subcellular localization in cells

    PMID:39653250

    Open questions at the time
    • Protease responsible for loop-mediated shedding not identified
    • Single-lab study
  17. 2025 Medium

    Systematically expanded the substrate landscape via proximity labeling, identifying new bisected substrates and a functional GLA-degradation axis in breast cancer.

    Evidence BASU/TurboID proximity labeling, glycopeptide MS, and breast cancer functional assays

    PMID:39851531

    Open questions at the time
    • Mechanism by which bisecting GlcNAc promotes GLA degradation unclear
    • Roles of GOLM2/CCDC134/ASPH/ERO1A modification untested
  18. 2025 Medium

    Defined acceptor-substrate specificity and kinetic preferences, showing GnT-III acts on multi-antennary and modified N-glycans, enabling asymmetric bisecting-glycan synthesis.

    Evidence Chemoenzymatic synthesis, kinetics, and glycan microarray screening (preprint)

    PMID:bio_10.1101_2025.06.26.661710

    Open questions at the time
    • Not peer-reviewed
    • In vitro specificity may not reflect cellular acceptor availability

Open questions

Synthesis pass · forward-looking unresolved questions
  • How bisecting GlcNAc on individual substrates mechanistically alters protein trafficking, stability, and signaling—and the physiological consequences of MGAT3 dysregulation in disease—remains incompletely defined.
  • No experimental high-resolution structure of the catalytic domain
  • Generalizable rules linking bisected glycan to substrate fate not established
  • In vivo disease causality from MGAT3 perturbation largely correlative

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5
Localization
GO:0005794 Golgi apparatus 2 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-1643685 Disease 3 R-HSA-392499 Metabolism of proteins 3
Partners
CD45CD82E-CADHERINGLAHAPTOGLOBINICAM-1NOTCH

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 Human GnT-III (MGAT3) encodes a 531-amino acid type II transmembrane protein that catalyzes the addition of N-acetylglucosamine in β1,4 linkage to the β-linked mannose of the trimannosyl core of N-linked sugar chains, producing a bisecting GlcNAc residue. The amino-terminal transmembrane domain and catalytic domain are conserved between human and rat. The gene maps to chromosome 22q13.1. cDNA cloning, open reading frame analysis, chromosomal mapping by fluorescence in situ hybridization (FISH) Journal of biochemistry High 8370666
1995 The mouse Mgat3 gene encodes GlcNAc-TIII and is expressed as a single-copy gene at high levels in kidney and brain. A sense-orientation ORF transfected into CHO cells confers GlcNAc-TIII enzymatic activity, demonstrating the ORF encodes the catalytic enzyme. Mouse Mgat3 maps to chromosome 15. Genomic cloning, mammalian expression transfection, enzymatic activity assay, Southern blot, FISH mapping Gene High 7590346
1997 Mgat3-deficient mice generated by Cre/loxP-mediated gene deletion lack GlcNAc-TIII activity and are deficient in E4-PHA-visualized GlcNAc-bisected N-linked oligosaccharides, yet are viable, fertile, and show no overt developmental, hematological, or organ morphology defects. This establishes that bisecting GlcNAc is dispensable for normal murine development and homeostasis. Gene targeting (Cre/loxP), enzymatic activity assay, lectin blotting, flow cytometry, histology Glycobiology High 9061364
2002 Active-site mutagenesis of rat GnT-III identified two conserved aspartate residues (Asp321 and Asp323) as absolutely required for catalytic activity based on sequence homology with snail β1,4GlcNAc transferase and β1,4Gal transferase-1. Overexpression of the catalytically inactive Asp323-substituted mutant suppressed endogenous GnT-III activity (dominant negative effect) and specifically blocked formation of bisected N-glycans without reducing endogenous GnT-III expression levels. Sequence homology analysis, site-directed mutagenesis, enzymatic activity assay, overexpression in Huh6 cells, N-glycan structural analysis European journal of biochemistry High 11784313
1995 GnT-III activity is elevated in CML blast crisis and multiple myeloma cells. Immunoprecipitation and lectin blot analysis showed that elevated GnT-III in KU812 (CML) cells results in increased bisecting GlcNAc on CD45, a major leukocyte surface glycoprotein, as its substrate. Enzymatic activity assay (HPLC), immunoprecipitation, Western/lectin blot with E4-PHA International journal of cancer Medium 7829256
2002 In GnT-III transgenic mice with DEN-induced hepatic tumors, glycomic analysis (2D gel electrophoresis, lectin blot, sequencing, immunoprecipitation) identified haptoglobin as a target glycoprotein modified by GnT-III-mediated bisecting GlcNAc addition, and GnT-III overexpression dramatically suppressed hepatic tumor incidence. Transgenic mouse model, 2D gel electrophoresis, lectin blot, sequence analysis, immunoprecipitation with E4-PHA lectin blot Free radical research Medium 12420740
2012 During epithelial-mesenchymal transition (EMT), Mgat3 promoter methylation causes dramatic reduction in Mgat3 expression and loss of GnT-III-mediated bisecting GlcNAc modification on E-cadherin; this is reversed during mesenchymal-epithelial transition (MET) by promoter demethylation. This identifies epigenetic regulation of Mgat3 as a mechanism controlling E-cadherin glycosylation during EMT/MET. Bisulfite sequencing, qPCR, Western blot, lectin blot, glycan analysis during TGF-β-induced EMT/MET in cell lines PloS one Medium 22427986
2012 All-trans-retinoic acid (ATRA) upregulates GnT-III expression via the ERK signaling pathway, causing bisecting GlcNAc modification of ICAM-1 N-glycans (shown by reduced ICAM-1 molecular mass reversible by PNGase F and by GnT-III siRNA knockdown). This GnT-III-dependent ICAM-1 glycan remodeling inhibits cell adhesion and trans-endothelial migration. siRNA knockdown, qPCR, gel mobility shift assay, PNGase F treatment, cell adhesion assay, trans-endothelial migration assay, ERK inhibitor treatment PloS one Medium 23300837
2014 In Fut8-deficient mouse embryonic fibroblasts (MEFs), loss of core fucose leads to upregulation of GnT-III expression via activation of Wnt/β-catenin signaling. A Wnt signaling inhibitor abrogates GnT-III upregulation. As a result, bisecting GlcNAc on β1-integrin and N-cadherin is increased; IgG1 glycan analysis by mass spectrometry confirms increased bisecting GlcNAc in Fut8-/- mouse serum in vivo. Mouse embryonic fibroblasts from Fut8-/- mice, gene expression analysis, Wnt inhibitor treatment, lectin blot, mass spectrometry of IgG glycans The Journal of biological chemistry Medium 24619415
2016 DNA methylation at the MGAT3 transcription start site represses MGAT3 expression; treatment with the DNA methyltransferase inhibitor 5-Aza restores MGAT3 expression coinciding with reduced promoter methylation. Bisecting GlcNAc on released N-glycans (detected by LC-ESI-qTOF-MS/MS) appears in ovarian cancer cells only after MGAT3 re-expression following demethylation, establishing promoter methylation as a direct mechanism controlling bisecting GlcNAc biosynthesis. 5-Aza treatment, bisulfite sequencing, LC-ESI-qTOF-MS/MS glycan analysis, expression analysis Oncotarget Medium 27429195
2017 GnT-III expression controls expansion of cancer stem cells (side-population cells) in epithelial ovarian carcinoma. shRNA suppression of GnT-III reduces Notch receptor levels and signaling more potently than pharmacologic γ-secretase inhibition, by redirecting Notch receptor to the lysosome rather than to the cell surface, identifying a novel mechanism whereby bisecting glycosylation controls Notch receptor trafficking. Stable shRNA knockdown, flow cytometry for side-population cells, Western blot, γ-secretase inhibitor comparison, lysosome localization assay, primary tumor-derived cells The Journal of biological chemistry Medium 28842505
2017 GLP-1 receptor agonists (exendin-4) downregulate aberrant GnT-III expression and bisecting GlcNAc levels in APP/PS1 mice and Aβ25-35-treated PC12 cells through the Akt/GSK-3β/β-catenin signaling pathway. β-catenin siRNA abolishes the effect of GLP-1RA on GnT-III, and PI3K inhibitor LY294002 attenuates these effects, establishing the Akt/GSK-3β/β-catenin axis as an upstream regulator of GnT-III expression. APP/PS1 transgenic mice, siRNA knockdown, PI3K inhibitor (LY294002), Western blot, phosphorylation analysis, behavioral testing Neuropharmacology Medium 29223528
2020 MGAT3-mediated glycosylation of CD82 at asparagine 157 is required for CD82-mediated inhibition of ovarian cancer cell migration and metastasis in vitro and in vivo. Mechanistically, glycosylated CD82 disrupts integrin α5β1-mediated cellular adhesion to fibronectin and inhibits integrin signaling-induced cytoskeletal rearrangements required for migration. MGAT3 was identified as the glycosyltransferase responsible for this CD82 glycosylation. Site-directed mutagenesis of CD82 glycosylation sites, in vitro migration/invasion assays, in vivo xenograft, integrin adhesion assays, Western blot, paired human tissue samples Theranostics High 32483464
2021 miR-23b directly targets the 3'-UTR of GnT-III mRNA (verified by dual-luciferase reporter assay), reducing GnT-III expression. miR-23b overexpression activates the Akt/GSK-3β signaling pathway to inhibit tau hyperphosphorylation and reduce oxidative stress in Alzheimer's disease models. Dual-luciferase reporter assay, bioinformatics, overexpression in Aβ1-42-induced mouse and PC12 cell models, Western blot Neuropharmacology Medium 34153312
2024 Structure-function analysis of GnT-III using AlphaFold2-based modeling and point mutagenesis identified E320 as the catalytic center of human GnT-III. A K346T mutant showed reduced in vitro activity but enhanced intracellular bisecting GlcNAc production; TurboID-based proximity labeling demonstrated that K346T is shifted to the cis-Golgi relative to wild-type, providing a mechanistic explanation for discordant in vitro vs. intracellular activity. Cycloheximide chase showed the K346T mutant has a shorter half-life. AlphaFold2 structure prediction, site-directed mutagenesis, in vitro activity assay, HPLC, UDP-Glo glycosyltransferase assay, glycomic analysis, TurboID proximity labeling, immunostaining, cycloheximide chase Biochimica et biophysica acta. General subjects Medium 38936637
2024 The middle loop (Loop) and C-terminal tail (Tail) of GnT-III play distinct functional roles: (1) deletion of Loop increases both in vitro and intracellular GnT-III activity, indicating Loop suppresses catalytic activity and contains the cleavage site for GnT-III shedding; (2) deletion of Tail reduces activity, increases ER localization, and accelerates protein degradation, indicating Tail is required for proper folding and Golgi localization. Deletion mutagenesis, HPLC activity assay, UDP-Glo assay, glycomic analysis, immunostaining for subcellular localization, degradation rate assay Biochimica et biophysica acta. General subjects Medium 39653250
2025 Proximity labeling with biotin ligases (BASU and TurboID) identified 116 and 189 proteins in the MGAT3 proximitome in HEK293T cells, with 17 shared with a bisecting GlcNAc-bearing proteome. Four novel substrates—GOLM2, CCDC134, ASPH, and ERO1A—were confirmed to bear bisecting GlcNAc modification. MGAT3-mediated bisecting GlcNAc on α-galactosidase A (GLA) promotes GLA degradation, thereby inhibiting breast cancer progression. TurboID and BASU proximity labeling, intact glycopeptide enrichment, mass spectrometry, Western blot, breast cancer functional assays Cells Medium 39851531
2025 Chemoenzymatic experiments established that GnT-III can act on bi-, tri-, and tetra-antennary N-glycans as substrates and preferentially modifies bi-antennary glycans (kinetic experiments). GnT-III also accepts N-glycans having a β1,2-GlcNTFA or GlcN3 moiety at the α1,2Man- or α1,6Man-antenna, enabling synthesis of asymmetric bisecting glycans. Chemoenzymatic synthesis, kinetic activity assays, glycan microarray screening bioRxivpreprint Medium bio_10.1101_2025.06.26.661710

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Survival of adult islet grafts from transgenic pigs with N-acetylglucosaminyltransferase-III (GnT-III) in cynomolgus monkeys. Xenotransplantation 120 15807771
1993 cDNA cloning, expression, and chromosomal localization of human N-acetylglucosaminyltransferase III (GnT-III). Journal of biochemistry 95 8370666
2012 Loss and recovery of Mgat3 and GnT-III Mediated E-cadherin N-glycosylation is a mechanism involved in epithelial-mesenchymal-epithelial transitions. PloS one 87 22427986
1997 Isolation, characterization and inactivation of the mouse Mgat3 gene: the bisecting N-acetylglucosamine in asparagine-linked oligosaccharides appears dispensable for viability and reproduction. Glycobiology 86 9061364
2006 Catalytic properties of MGAT3, a putative triacylgycerol synthase. Journal of lipid research 76 17170429
2017 GLP-1 receptor agonists downregulate aberrant GnT-III expression in Alzheimer's disease models through the Akt/GSK-3β/β-catenin signaling. Neuropharmacology 52 29223528
2020 MGAT3-mediated glycosylation of tetraspanin CD82 at asparagine 157 suppresses ovarian cancer metastasis by inhibiting the integrin signaling pathway. Theranostics 47 32483464
2014 The absence of core fucose up-regulates GnT-III and Wnt target genes: a possible mechanism for an adaptive response in terms of glycan function. The Journal of biological chemistry 43 24619415
2021 Exosomal miR‑663b exposed to TGF‑β1 promotes cervical cancer metastasis and epithelial‑mesenchymal transition by targeting MGAT3. Oncology reports 40 33649791
2017 The glycosyltransferase GnT-III activates Notch signaling and drives stem cell expansion to promote the growth and invasion of ovarian cancer. The Journal of biological chemistry 40 28842505
1995 Cloning and chromosomal mapping of the mouse Mgat3 gene encoding N-acetylglucosaminyltransferase III. Gene 40 7590346
2020 True significance of N-acetylglucosaminyltransferases GnT-III, V and α1,6 fucosyltransferase in epithelial-mesenchymal transition and cancer. Molecular aspects of medicine 39 33010941
2021 MicroRNA-23b attenuates tau pathology and inhibits oxidative stress by targeting GnT-III in Alzheimer's disease. Neuropharmacology 30 34153312
2018 Promoter methylation of the MGAT3 and BACH2 genes correlates with the composition of the immunoglobulin G glycome in inflammatory bowel disease. Clinical epigenetics 30 29991969
2016 Epigenetic activation of MGAT3 and corresponding bisecting GlcNAc shortens the survival of cancer patients. Oncotarget 30 27429195
1995 High expression of UDP-N-acetylglucosamine: beta-D mannoside beta-1,4-N-acetylglucosaminyltransferase III (GnT-III) in chronic myelogenous leukemia in blast crisis. International journal of cancer 29 7829256
2018 MiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat3. Scientific reports 28 29743543
2018 The glycomic effect of N-acetylglucosaminyltransferase III overexpression in metastatic melanoma cells. GnT-III modifies highly branched N-glycans. Glycoconjugate journal 27 29502191
2011 The acyl coenzymeA:monoacylglycerol acyltransferase 3 (MGAT3) gene is a pseudogene in mice but encodes a functional enzyme in rats. Lipids 27 21312067
2016 DNA hypomethylation upregulates expression of the MGAT3 gene in HepG2 cells and leads to changes in N-glycosylation of secreted glycoproteins. Scientific reports 26 27073020
2002 A catalytically inactive beta 1,4-N-acetylglucosaminyltransferase III (GnT-III) behaves as a dominant negative GnT-III inhibitor. European journal of biochemistry 23 11784313
1995 Changes of beta-1,4-N-acetylglucosaminyltransferase III (GnT-III) in patients with leukaemia. Glycoconjugate journal 21 7496137
2012 All-trans-retinoic acid modulates ICAM-1 N-glycan composition by influencing GnT-III levels and inhibits cell adhesion and trans-endothelial migration. PloS one 19 23300837
2020 Suppression of MGAT3 expression and the epithelial-mesenchymal transition of lung cancer cells by miR-188-5p. Biomedical journal 17 35166206
2016 Biochemical characterization of human acyl coenzyme A: 2-monoacylglycerol acyltransferase-3 (MGAT3). Biochemical and biophysical research communications 17 27184406
2019 Endogenous intronic antisense long non-coding RNA, MGAT3-AS1, and kidney transplantation. Scientific reports 11 31611608
2002 A glycomic approach to hepatic tumors in N-acetylglucosaminyltransferase III (GnT-III) transgenic mice induced by diethylnitrosamine (DEN): identification of haptoglobin as a target molecule of GnT-III. Free radical research 10 12420740
2020 Prospective Study of Long Noncoding RNA, MGAT3-AS1, and Viremia of BK Polyomavirus and Cytomegalovirus in Living Donor Renal Transplant Recipients. Kidney international reports 9 33305115
2024 Circ_0070934 promotes MGAT3 expression and inhibits epithelial-mesenchymal transition in bronchial epithelial cells by sponging miR-199a-5p. Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology 4 38521909
2024 The K346T mutant of GnT-III bearing weak in vitro and potent intracellular activity. Biochimica et biophysica acta. General subjects 4 38936637
2020 Associations between genetic variants of KIF5B, FMN1, and MGAT3 in the cadherin pathway and pancreatic cancer risk. Cancer medicine 4 33200553
2025 Proximity Labeling-Based Identification of MGAT3 Substrates and Revelation of the Tumor-Suppressive Role of Bisecting GlcNAc in Breast Cancer via GLA Degradation. Cells 2 39851531
2025 MGAT3 and MGAT5 overexpression alters the protein cargo of extracellular vesicles released by metastatic melanoma cells. Biochemical and biophysical research communications 0 40199132
2025 Downregulation of MGAT3 Promotes Benzo[a]pyrene-Mediated Lung Carcinogenesis by Regulating Cell Invasion and Migration Activity. ACS omega 0 40352502
2024 Functions of unique middle loop and C-terminal tail in GnT-III activity and secretion. Biochimica et biophysica acta. General subjects 0 39653250
2019 N-Acetylglucosaminyltransferase III (GnT-III) but not N-Acetylgalactosaminyltransferase-6 and 8 are Differentially Expressed in Invasive and In Situ Ductal Carcinoma of the Breast. Pathology oncology research : POR 0 30689164

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