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Merck

G4048

Sigma-Aldrich

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

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

Synonym(e):

Anti-Glucose transporter 4, Anti-SLC2A4

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About This Item

UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

rabbit

Konjugat

unconjugated

Antikörperform

affinity isolated antibody

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Form

buffered aqueous solution

Mol-Gew.

antigen ~58 kDa

Speziesreaktivität

mouse, human

Konzentration

~1.5 mg/mL

Methode(n)

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

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

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

Allgemeine Beschreibung

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.

Anwendung

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.

Biochem./physiol. Wirkung

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

Physikalische Form

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

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

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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)
Signaling, cytoskeletal and membrane mechanisms regulating GLUT4 exocytosis
Hoffman NJ and Elmendorf JS
Trends in Endocrinology and Metabolism, 22(3), 110-116 (2011)
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
Alexander F Rowland et al.
Traffic (Copenhagen, Denmark), 12(6), 672-681 (2011-03-16)
One of the most important metabolic actions of insulin is catalysing glucose uptake into skeletal muscle and adipose tissue. This is accomplished via activation of the phosphatidylinositol-3-kinase/Akt signalling pathway and subsequent translocation of GLUT4 from intracellular storage vesicles to the
Stephan Nieuwoudt et al.
American journal of physiology. Cell physiology, 313(5), C575-C583 (2017-08-25)
We are interested in understanding mechanisms that govern the protective role of exercise against lipid-induced insulin resistance, a key driver of type 2 diabetes. In this context, cell culture models provide a level of abstraction that aid in our understanding

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