Monoclonal Anti-EDEM3 (mouse IgG1 isotype) is derived from the hybridoma EDEM3-1 produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with a synthetic peptide corresponding to a fragment of human EDEM3 conjugated to KLH.
Three EDEM homologs, EDEM1, EDEM2 and EDEM3 have been identified, which are transcriptionally upregulated upon ER stress by the activated IRE1/Xbp-1 branch.
Application
Monoclonal Anti-EDEM3 antibody produced in mouse has been used in immunoblotting.
Biochem/physiol Actions
EDEM3 (ER degradation enhancer, mannosidase α-like 3), a soluble EDEM homolog, enhances glycoprotein endoplasmic reticulum-associated degradation (ERAD) and mannose trimming. EDEM3 accelerates ERAD of misfolded glycoproteins as well, but in ontrast to EDEM1, it greatly stimulates mannosidase trimming in vivo.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
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.
Sequential mannose trimming of N-glycan, from M9 to M8B and then to oligosaccharides exposing the α1,6-linked mannosyl residue (M7A, M6, and M5), facilitates endoplasmic reticulum-associated degradation of misfolded glycoproteins (gpERAD). We previously showed that EDEM2 stably disulfide-bonded to the thioredoxin
Chembiochem : a European journal of chemical biology, 18(11), 1027-1035 (2017-04-04)
Within the endoplasmic reticulum, immature glycoproteins are sorted into secretion and degradation pathways through the sequential trimming of mannose residues from Man9 GlcNAc2 to Man5 GlcNAc2 by the combined actions of assorted α-1,2-mannosidases. It has been speculated that specific glycoforms
The application of forward genetic screens to cultured human cells represents a powerful method to study gene function. The repurposing of the bacterial CRISPR/Cas9 system provides an effective method to disrupt gene function in mammalian cells, and has been applied
The field of endoplasmic reticulum (ER) stress in mammalian cells has expanded rapidly during the past decade, contributing to understanding of the molecular pathways that allow cells to adapt to perturbations in ER homeostasis. One major mechanism is mediated by
Questions
Reviews
★★★★★ No rating value
Active Filters
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
