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SAB4502803

Sigma-Aldrich

Anti-GLUT1 antibody produced in rabbit

affinity isolated antibody

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Synonym(s):
GLUT-1, Glucose transporter type 1 erythrocyte/brain, HepG2 glucose transporter, SLC2A1, Solute carrier family 2 facilitated glucose transporter member 1
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 54 kDa

species reactivity

mouse, human, rat

concentration

~1 mg/mL

technique(s)

ELISA: 1:40000
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... SLC2A1(6513)

General description

Anti-GLUT1 Antibody detects endogenous levels of total GLUT1 protein.
GLUT1 (Glucose transporter type 1) gene is located on human chromosome 1p34.2. It is expressed in cerebral endothelial cells.

Immunogen

The antiserum was produced against synthesized peptide derived from human GLUT1.

Immunogen Range: 441-490

Application

Anti-GLUT1 antibody produced in rabbit has been used
  • for protein extraction
  • in western blotting
  • for immunohistochemistry

Anti-GLUT1, C-Terminal antibody is suitable for use in western blot and immunohistochemistry.

Biochem/physiol Actions

GLUT1 (Glucose transporter type 1) functions as a receptor for human T-cell leukemia virus (HTLV) I and II. It plays a key role in HTLV-envelope mediated infection. GLUT1 is associated with paroxysmal exertion-induced dyskinesia. Glut1 may regulate cerebral microvasculature, proliferation of endothelial cells and the development of junctional complexes of the BBB (blood-brain barrier). It transports glucose across the BBB.
GLUT1 is a membrane protein that regulates the facilitative transport of glucose across the cells. Mutations in the gene encoding GLUT1 have been linked to epilepsy and diabetic nephropathy . Increased expression of GLUT1 has been associated with tumor differentiation in breast and endometrial cancers, whereas decreased GLUT1 function causes GLUT1 deficiency syndrome . Anti-GLUT1, C-Terminal antibody can be used to detect endogenous levels of total GLUT1 protein. The antibody specifically reacts with GLUT1 in mice, rats and humans.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Physical form

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

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.

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

常规特殊物品

Certificates of Analysis (COA)

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The ubiquitous glucose transporter GLUT-1 is a receptor for HTLV
Manel N, et al.
Cell, 115(4), 449-459 (2003)
Glucose modulation induces reactive oxygen species and increases P-glycoprotein-mediated multidrug resistance to chemotherapeutics
Seebacher NA, et al.
British Journal of Pharmacology, 172(10), 2557-2572 (2015)
Paroxysmal dyskinesias
Bhatia KP
Movement Disorders, 26(6), 1157-1165 (2011)
Yang Li et al.
Molecular metabolism, 66, 101630-101630 (2022-11-08)
Bone is a highly dynamic organ that undergoes constant bone formation and remodeling, and glucose as a major nutrient is necessary for bone formation and remodeling. Retinoblastoma (Rb1) is a critical regulator of mesenchymal stem cells (MSCs) fate, but how
Glut1/SLC2A1 is crucial for the development of the blood-brain barrier in vivo.
Zheng P P, et al.
Annals of Neurology, 68(6), 835-844 (2010)

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