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Key Documents

G4048

Sigma-Aldrich

Anti-GLUT4 (C-terminal) antibody produced in rabbit

~1.5 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonyme(s) :

Anti-Glucose transporter 4, Anti-SLC2A4

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~58 kDa

Espèces réactives

mouse, human

Concentration

~1.5 mg/mL

Technique(s)

indirect immunofluorescence: 15-20 μg/mL using C2C12 cells
western blot: 1-2 μg/mL using C2C12 cell lysate and HepG2 cell lysate

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... SLC2A4(6517)
mouse ... Slc2a4(20528)
rat ... Slc2a4(25139)

Catégories apparentées

Description générale

The GLUT4 (glucose transporter 4) gene, also known as SLC2A4 (solute carrier family 2 member 4) is mapped to human chromosome 17p13.1.The expression of GLUT4 (glucose transporter 4) is the highest in skeletal and adipose tissue.

Application

Anti-GLUT4 (C-terminal) antibody may be used for immunoblotting at a working concentration of 1-2 μg/ml in whole cell lysate of C2C12 and HepG2 cells. A working dilution of 1:3000 was used for immunoblotting in whole cell lysate of HEK-293 cells. . Anti-GLUT4 (C-terminal) antibody has also been used for immunoblotting in CHO-K1 cells. Antibody concentration of 15-20 μg/ml is recommended for immunofluorescence in C2C12 cells.
Anti-GLUT4 (C-terminal) antibody produced in rabbit has been used in western blotting and immunofluorescence assay.

Actions biochimiques/physiologiques

GLUT4 is an insulin-regulated glucose transporter that facilitates the uptake of glusose by fat and muscle cells. Generally restricted to storage vesicles, GLUT4 translocates to the plasma membrane in response to insulin stimulation. The vital function of GLUT4 is regulation of glucose utilization by the cells. Following meal consumption, insulin secreted by the pancreas binds to receptors on the muscle and adipose and activates the PI3K-Akt pathway. Activation of this pathway triggers the secretion of GLUT4 from the vesicles that translocate to the plasma membrane. An overall decrease in the expression of GLUT4 results in diabetes and a selective disruption of GLUT4, in skeletal or adipose tissue, results in insulin resistance

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

10 - Combustible liquids

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Adelle C F Coster et al.
Traffic (Copenhagen, Denmark), 5(10), 763-771 (2004-09-10)
The insulin-sensitive glucose transporter GLUT4 mediates the uptake of glucose into adipocytes and muscle cells. In this study we have used a novel 96-well plate fluorescence assay to study the kinetics of GLUT4 trafficking in 3T3-L1 adipocytes. We have found
Signaling, cytoskeletal and membrane mechanisms regulating GLUT4 exocytosis
Hoffman NJ and Elmendorf JS
Trends in Endocrinology and Metabolism, 22(3), 110-116 (2011)
Effect of tnf-alpha on caveolin-1 expression and insulin signaling during adipocyte differentiation and in mature adipocytes
Palacios OS, et al.
Cellular Physiology and Biochemistry, 36(4), 1499-1516 (2015)
Endocrinological abnormalities are a main feature of 17p13. 1 microduplication syndrome: a new case and literature review
Maini I, et al.
Molecular Syndromology, 7(6), 337-343 (2016)
Retinoblastoma protein knockdown favors oxidative metabolism and glucose and fatty acid disposal in muscle cells
Petrov PD, et al.
Journal of Cellular Physiology, 231(3), 708-718 (2016)

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