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Key Documents

SAB1401244

Sigma-Aldrich

Monoclonal Anti-MGAT5 antibody produced in mouse

clone 3E9, purified immunoglobulin, buffered aqueous solution

Synonym(s):

GNT-V, GNT-VA

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

3E9, monoclonal

form

buffered aqueous solution

species reactivity

human

technique(s)

capture ELISA: suitable
western blot: 1-5 μg/mL

isotype

IgG2aκ

NCBI accession no.

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... MGAT5(4249)

General description

This gene encodes mannosyl (alpha-1,6-)-glycoprotein beta-1,6-N-acetyl-glucosaminyltransferase, a glycosyltransferase involved in the synthesis of protein-bound and lipid-bound oligosaccharides. Alterations of the oligosaccharides on cell surface glycoproteins cause significant changes in the adhesive or migratory behavior of a cell. Increase in the encoded protein′s activity may correlate with the progression of invasive malignancies. (provided by RefSeq)

Immunogen

MGAT5 (NP_002401, 642 a.a. ~ 739 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.

Sequence
LAEPGQSCKQVCQESQLICEPSFFQHLNKDKDMLKYKVTCQSSELAKDILVPSFDPKNKHCVFQGDLLLFSCAGAHPRHQRVCPCRDFIKGQVALCKD

Biochem/physiol Actions

MGAT5 (mannosyl (α-1,6-)-glycoprotein β-1,6-N-acetylglucosaminyltransferase) is involved in the biosynthesis of N-linked glycoproteins. It catalyzes the formation of β
1,6-branched N-glycans by N-acetyl-d-glucosamine transfer. MGAT5 plays a significant role in invasion and metastasis of various cancer, including glioma and hepatocellular carcinoma. It is also known to be associated with multiple sclerosis and liver fibrosis. Increased radiosensitivity of cancer cells is observed upon MGAT5 inhibition.

Physical form

Solution in phosphate buffered saline, pH 7.4

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Arisa Kato et al.
Experimental dermatology, 24(8), 585-590 (2015-04-17)
Oligosaccharide modification by N-acetylglucosaminyltransferase-V (GnT-V), which catalyses the formation of β1,6 GlcNAc (N-acetylglucosamine) branches on N-glycans, is associated with various pathologies, such as cancer metastasis, multiple sclerosis and liver fibrosis. In this study, we demonstrated the involvement of GnT-V in
Oligosaccharide modification by N-acetylglucosaminyltransferase-V in macrophages are involved in pathogenesis of bleomycin-induced scleroderma.
Kato A
Experimental Dermatology, 24(8), 585-590 (2015)
A Loukola et al.
Molecular psychiatry, 19(5), 615-624 (2013-06-12)
Smoking is a major risk factor for several somatic diseases and is also emerging as a causal factor for neuropsychiatric disorders. Genome-wide association (GWA) and candidate gene studies for smoking behavior and nicotine dependence (ND) have disclosed too few predisposing
Effect of GnT-V knockdown on the proliferation, migration and invasion of the SMMC7721/R human hepatocellular carcinoma drug-resistant cell line.
Li B
Molecular Medicine Reports, 13(1), 469-476 (2016)
Radiosensitisation of human glioma cells by inhibition of ?1,6-GlcNAc branched N-glycans.
Shen L
Tumour Biology : the Journal of the International Society For Oncodevelopmental Biology and Medicine, 37(4), 4909-4918 (2016)

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