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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

Sinónimos:

Anti-Glucose transporter 4, Anti-SLC2A4

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About This Item

Código UNSPSC:
12352203
NACRES:
NA.41

origen biológico

rabbit

Nivel de calidad

conjugado

unconjugated

forma del anticuerpo

affinity isolated antibody

tipo de anticuerpo

primary antibodies

clon

polyclonal

Formulario

buffered aqueous solution

mol peso

antigen ~58 kDa

reactividad de especies

mouse, human

concentración

~1.5 mg/mL

técnicas

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

Nº de acceso UniProt

Condiciones de envío

dry ice

temp. de almacenamiento

−20°C

modificación del objetivo postraduccional

unmodified

Información sobre el gen

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

Descripción general

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.

Aplicación

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.

Acciones bioquímicas o fisiológicas

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

Forma física

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

Cláusula de descargo de responsabilidad

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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Código de clase de almacenamiento

10 - Combustible liquids

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable


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Visite la Librería de documentos

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)
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)
Signaling, cytoskeletal and membrane mechanisms regulating GLUT4 exocytosis
Hoffman NJ and Elmendorf JS
Trends in Endocrinology and Metabolism, 22(3), 110-116 (2011)
Expression of Caveolin 1 is enhanced by DNA demethylation during adipocyte differentiation. status of insulin signaling
Palacios OS, et al.
Testing, 9(4), e95100-e95100 (2014)

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