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Merck
CN

G4048

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

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

Synonym(s):

Anti-Glucose transporter 4, Anti-SLC2A4

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About This Item

NACRES:
NA.41
UNSPSC Code:
12352203
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Product Name

Anti-GLUT4 (C-terminal) antibody produced in rabbit, ~1.5 mg/mL, affinity isolated antibody, buffered aqueous solution

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~58 kDa

species reactivity

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

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

Gene Information

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

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.

Biochem/physiol Actions

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

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.

General description

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.

Physical form

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

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Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable

Regulatory Information

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Jacqueline Stöckli et al.
Journal of cell science, 124(Pt 24), 4147-4159 (2012-01-17)
GLUT4 is an insulin-regulated glucose transporter that is responsible for insulin-regulated glucose uptake into fat and muscle cells. In the absence of insulin, GLUT4 is mainly found in intracellular vesicles referred to as GLUT4 storage vesicles (GSVs). Here, we summarise
Sequence Determinants of GLUT1-mediated Accelerated-Exchange Transport - Analysis by Homology-Scanning Mutagenesis
Vollers SS and Carruthers A
The Journal of Biological Chemistry, doi: 10-doi: 10 (2012)
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
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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