MGAT5 Antibody
Description
MGAT5 Antibody: Definition and Purpose
The MGAT5 antibody is a monoclonal or polyclonal immunoglobulin designed to specifically bind to the MGAT5 protein. Its primary purpose is to detect MGAT5 expression in cells, tissues, or biological samples via techniques such as:
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Western blotting (WB)
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Immunofluorescence (IF)
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Flow cytometry
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Immunohistochemistry (IHC)
MGAT5 antibodies are used to study N-glycosylation patterns, cancer progression, and immune modulation, particularly in the context of immunotherapy resistance .
Role in Cancer Progression and Immunotherapy
MGAT5 overexpression is linked to aggressive cancer phenotypes due to its role in synthesizing β-1,6-branched N-glycans. These glycans bind galectins, stabilizing pro-survival receptors and inhibiting immune recognition .
Key Studies:
Detection Methods and Validation
MGAT5 antibodies are validated for diverse techniques:
Challenges:
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Variable Band Sizes: ab87977 detects 55 kDa and 95 kDa bands, suggesting glycosylation or alternative splicing .
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IHC Limitations: Commercial antibodies for IHC are sparse; polyclonal antibodies (e.g., CSB-PA600992) may offer better sensitivity .
Future Directions and Therapeutic Implications
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Biomarker Development:
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Targeted Therapies:
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Diagnostic Tools:
Product Specs
Target Background
This antibody targets MGAT5 (N-acetylglucosaminyltransferase V), an enzyme that catalyzes the addition of N-acetylglucosamine (GlcNAc) in a β1-6 linkage to the α-linked mannose of biantennary N-linked oligosaccharides. This crucial step in the biosynthesis of branched, complex-type N-glycans impacts various glycoproteins, including EGFR, TGFβR (TGF-beta receptor), and CDH2. MGAT5's influence on complex N-glycan biosynthesis plays a significant role in activating cellular signaling pathways, reorganizing the actin cytoskeleton, mediating cell-cell adhesion, and regulating cell migration. Specifically, MGAT5-dependent EGFR N-glycosylation enhances EGFR interaction with LGALS3, preventing rapid EGFR endocytosis and prolonging its signaling. It's also essential for efficient interaction between TGFβ1 and its receptor. Furthermore, MGAT5 enhances activation of intracellular signaling pathways by various growth factors (FGF2, PDGF, IGF, TGFβ1, and EGF). MGAT5-dependent CDH2 N-glycosylation inhibits CDH2-mediated homotypic cell-cell adhesion and regulates downstream signaling. MGAT5 promotes cell migration, contributes to inflammatory response regulation, and, through TCR N-glycosylation, influences TCR interaction with LGALS3, modulating TCR-mediated responses to antigens. It's required for normal leukocyte extravasation and accumulation at inflammatory sites, inhibits monocyte adhesion to the endothelium and diapedesis, and promotes umbilical vein endothelial cell proliferation and angiogenesis, at least partly by promoting FGF2 release from the extracellular matrix.
Numerous studies highlight the significant role of MGAT5 in various biological processes and disease states. Key findings include:
- Homology modeling provides insights into MGAT5's catalytic mechanism and aids in inhibitor design. (PMID: 26821880)
- Oxidative stress upregulates MGAT5 expression via the focal adhesion kinase-ERK signaling pathway, impacting endothelial cell function and potentially contributing to preeclampsia pathogenesis. (PMID: 27334383)
- PTPα is identified as a novel MGAT5 substrate, potentially influencing breast cancer cell migration. (PMID: 27965091)
- Targeting N-linked β1,6-GlcNAc branches, regulated by MGAT5, shows promise as a therapeutic strategy in glioblastoma treatment. (PMID: 26526581)
- MGAT5 knockdown significantly suppresses proliferation, migration, and invasion of SMMC7721/R cells. (PMID: 26531171)
- MGAT5 may inhibit trophoblast cell invasion and migration during early pregnancy, potentially via MMP2/9 regulation. (PMID: 26349781)
- MGAT5 plays a crucial role in hexosamine-induced activation of TGF-β signaling and osteogenic differentiation. (PMID: 26583147)
- MGAT5 is implicated in early spontaneous miscarriage. (PMID: 26109616)
- MGAT5 overexpression accelerates tumor growth. (PMID: 26293457)
- High MGAT5 expression is observed in infiltrating cells in scleroderma patients. (PMID: 25876794)
- MGAT5 expression is studied in uveal and cutaneous melanoma cells. (PMID: 26098720)
- MGAT5 increases amino acid uptake, glycolytic and TCA intermediates, and HEK293 cell growth. (PMID: 25395405)
- Reduced MGAT5 expression contributes to ulcerative colitis pathogenesis by affecting TCR N-glycosylation. (PMID: 24334766)
- MGAT5-mediated β1-6-GlcNAc branching and subsequent EGFR activation are implicated in PAK1-induced anoikis resistance in hepatoma cells. (PMID: 23811795)
- MGAT5 regulation in gastric cancer holds potential clinical applications. (PMID: 24399258)
- MGAT5 plays a significant role in gastric cancer metastasis and invasion. (PMID: 23563846)
- MGAT5 expression, combined with TNM or Kiel staging, improves overall survival prediction. (PMID: 23107376)
- MGAT5 directs cancer progression by modulating matrix metalloproteinases (MMPs). (PMID: 23357422)
- MGAT5 variants (rs4953911 and rs3814022) correlate with lower N-glycan branching, reduced surface CTLA-4, and multiple sclerosis. (PMID: 23351704)
- Aberrant β1,6-branches on CD147, due to MGAT5 overexpression, are crucial for MMP induction in SMMC-7721 cells. (PMID: 23005037)
- MGAT5 may be a potential target for predicting nasopharyngeal carcinoma response to radiotherapy. (PMID: 22780953)
- MGAT5 expression is positively related to malignancy in hepatocellular carcinoma (HCC). (PMID: 22537550)
- Genetic studies identified associations between MGAT5 and glycosylation traits. (PMID: 21908519)
- Inhibition of MGAT5 expression inhibits PC-3 cell proliferation. (PMID: 20584650)
- MGAT5 expression is positively correlated with malignancy in nasopharyngeal carcinoma. (PMID: 21676538)
- MGAT5 may be a therapeutic target for pulmonary adenocarcinoma. (PMID: 21631992)
- The MGAT5 rs1257169(G) allele is associated with lower multiple sclerosis severity. (PMID: 21115203)
- MGAT5 has a pH optimum of 6.5-7.0 and is fully active without exogenous cations. (PMID: 19846580)
- MGAT5 may decrease hepatoma cell adhesion and promote proliferation through RPTPκ. (PMID: 19911372)
- MGAT5's prometastatic effect involves modifying and stabilizing active matriptase. (PMID: 11864986)
- A secreted form of MGAT5 induces tumor angiogenesis independently of its glycosyltransferase activity. (PMID: 11872751)
- Low MGAT5 expression is associated with shorter survival in pStage I non-small cell lung cancer. (PMID: 15014031)
- MGAT5 affects the expression of other glycosyltransferases involved in sialyl Lewis X antigen synthesis. (PMID: 15044007)
- MGAT5 activity is upregulated in rheumatoid arthritis and vitamin D3-treated hepatoma cells. (PMID: 15313475)
- MGAT5 may contribute to placentation by regulating trophoblast cell invasion. (PMID: 15809094)
- Blocking MGAT5 expression impairs chaperone and N-glycan-synthesizing enzyme functions, causing endoplasmic reticulum stress. (PMID: 16467879)
- Low MGAT5 expression is associated with low malignant potential and good prognosis in bladder cancer. (PMID: 16638859)
- MGAT5-mediated glycosylation directs integrin β1 stability, promoting cell migration and invasion. (PMID: 16924681)
- MGAT5 may regulate glucose uptake by modifying GLUT1 glycosylation. (PMID: 17451637)
- MGAT5 expression is decreased in drug-resistant cancer cells. (PMID: 17488527)
- TIMP-1 is identified as a target protein for MGAT5 in human colon cancer. (PMID: 17878270)
- High MGAT5 expression correlates with unfavorable clinical outcomes. (PMID: 17971775)
- MGAT5 knockdown attenuates prostate cancer cell metastasis. (PMID: 18649738)
- MGAT5 expression correlates with poor prognosis in gastric cancer due to metastasis. (PMID: 18931531)
- MGAT5 knockdown inhibits ligand-induced EGFR internalization, affecting downstream signaling and invasiveness. (PMID: 19225046)
- MGAT5 overexpression modifies RPTPκ N-glycans and decreases its protein level. (PMID: 19236842)
- High MGAT5 expression is associated with mucinous ovarian tumors. (PMID: 19787216)
