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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

Synonyme(s) :

Anti-ER degradation enhancer, mannosidase α-like 3

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

mouse

Conjugué

unconjugated

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

EDEM3-1, monoclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~120 kDa

Espèces réactives

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

Numéro d'accès UniProt

Q9BZQ6

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

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

Description générale

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.

Actions biochimiques/physiologiques

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.

Forme physique

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Clause de non-responsabilité

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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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

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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