MOGS Antibodies

AND MOGS ELISA kits, MOGS Proteins

Many biological assays use antibodies to detect MOGS, such as Western Blot (WB), ELISA, Flow Cytometry, Immunocytochemistry (IHC). These antibodies can be polyclonal or monoclonal, and react with MOGS in Human, Mouse, Rat, and many other animal samples. Boster Bio use mainly mouse and rabbit to develop MOGS antibodies...

We validate the specificity of these antibodies to MOGS by testing them on tissues known to express MOGS positively and negatively. Browse below to find the MOGS antibody that suites your experiment. We have 1 of these antibodies and many publications and validation images.

If you cannot find antibodies that fit your needs, contact us for making custom antibodies. We have a full suite of custom antibody services covering from research to diagnostic and therapeutic applications.

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MOGS Infographic by Boster Bio

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Anti-MOGS Antibody

Human, Mouse, Rat

$405
Cat # A08252
100ul

MOGS Overview

Facts about Mannosyl-oligosaccharide glucosidase.

MOGS 3D structure. Source: alphafold

Mannosyl-oligosaccharide glucosidase (MOGS)

Cleaves the distal alpha 1,2-linked glucose residue from the Glc(3)Man(9)GlcNAc(2) oligosaccharide precursor in a highly specific manner. .

Gene Information

Human
Gene Name:	MOGS
Uniprot:	Q13724
Entrez:	7841

Family

Belongs to:

glycosyl hydrolase 63 family

Alternative Names

GCS1; glucosidase I; mannosyl-oligosaccharide glucosidase; processing A-glucosidase I

Molecular Weight

Mass (kDA):
91.918 kDA

Genomic Context


Human

Location:	2p13.1
Sequence:	2; NC_000002.12 (74461057..74465382, complement)

Subcellular Localizations

Endoplasmic reticulum membrane; Single-pass type II membrane protein.

Diseases

Type IIb congenital disorder of glycosylation (CDGIIb)

PTMs

Oxidation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/MOGS

References

PMID: 7635146 by Kalz-Fueller B., et al. Cloning and expression of glucosidase I from human hippocampus.

PMID: 10788335 by De Praeter C.M., et al. A novel disorder caused by defective biosynthesis of N-linked oligosaccharides due to glucosidase I deficiency.