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E0409

Sigma-Aldrich

Monoclonal Anti-EDEM3 antibody produced in mouse

~1.0 mg/mL, clone EDEM3-1, purified immunoglobulin, buffered aqueous solution

Synonym(s):

Anti-ER degradation enhancer, mannosidase α-like 3

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

200

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

EDEM3-1, monoclonal

form

buffered aqueous solution

mol wt

antigen ~120 kDa

species reactivity

rat, mouse, human

concentration

~1.0 mg/mL

technique(s)

western blot: 1-2 μg/mL using whole extract of mouse 3T3 or rat NRK cells

UniProt accession no.

Q9BZQ6

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... EDEM3(80267)
mouse ... Edem3(66967)
rat ... Edem3(289085)

General description

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.

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Storage Class Code

12 - Non Combustible Liquids

WGK

nwg

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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Redundant and Antagonistic Roles of XTP3B and OS9 in Decoding Glycan and Non-glycan Degrons in ER-Associated Degradation
van der Goot AT, et al.
Molecular Cell, 70(3), 516-530 e6-516-530 e6 (2018)
Ginto George et al.
eLife, 10 (2021-10-27)
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
Taiki Kuribara et al.
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
Richard T Timms et al.
Nature communications, 7, 11786-11786 (2016-06-11)
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
Min Ni et al.
FEBS letters, 581(19), 3641-3651 (2007-05-08)
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

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