HPA031345
Anti-SLC2A1 antibody produced in rabbit
affinity isolated antibody, buffered aqueous glycerol solution
Synonym(s):
Anti-DYT18, Anti-GLUT, Anti-GLUT1, Anti-HTLVR
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About This Item
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biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous glycerol solution
species reactivity
human
enhanced validation
orthogonal RNAseq
Learn more about Antibody Enhanced Validation
technique(s)
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:1000-1:2500
immunogen sequence
GRTFDEIASGFRQGGASQSDKTPEELFHP
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... SLC2A1(6513)
Related Categories
General description
The SLC2A1 (solute carrier family 2 member 1) gene is 35kb in length and is mapped to human chromosome 1p35 → p31.3. The gene contains 10 exons and nine introns. Its mRNA is found to be expressed in several tissues. It is highly expressed in cerebral endothelial cells and the encoded protein has 12 transmembrane domains.
Immunogen
solute carrier family 2 (facilitated glucose transporter), member 1
Application
Anti-SLC2A1 antibody produced in rabbit has been used in immunohistochemistry.
Biochem/physiol Actions
The SLC2A1 (solute carrier family 2 member 1) gene, also referred to as GLUT1, encodes protein that is mainly involved in the transport of D-glucose across the blood-brain barrier. Mutation in this gene causes Glut-1 deficiency syndrome, which is characterized by reduced cerebrospinal fluid glucose concentrations (hypoglycorrhachia) and reduced erythrocyte glucose transporter activities in the patients along with infantile seizures, acquired microcephaly and developmental delay. It has been found to be critical in the development of the blood-brain barrier. Mutation in this gene has also been associated with paroxysmal exercise-induced dyskinesia and epilepsy.
Features and Benefits
Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.
Every Prestige Antibody is tested in the following ways:
Every Prestige Antibody is tested in the following ways:
- IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
- Protein array of 364 human recombinant protein fragments.
Linkage
Corresponding Antigen APREST87043
Physical form
Solution in phosphate buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide.
Legal Information
Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany
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.
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Product No.
Description
Pricing
Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Qi Wang et al.
Brain : a journal of neurology, 145(12), 4474-4488 (2022-07-06)
Alzheimer's disease is a neurodegenerative disorder that causes age-dependent neurological and cognitive declines. The treatments for Alzheimer's disease pose a significant challenge, because the mechanisms of disease are not being fully understood. Malfunction of the blood-brain barrier is increasingly recognized
Yang Chen et al.
Heliyon, 10(12), e33077-e33077 (2024-07-12)
Dysfunction of the blood-brain barrier (BBB) has been increasingly recognised as a critical early event in Alzheimer's disease (AD) pathophysiology. Central to this mechanism is the impaired function of brain endothelial cells (BECs), the primary structural constituents of the BBB
Mutational analysis of GLUT1 (SLC2A1) in Glut-1 deficiency syndrome.
Wang D, et al.
Human Genetics, 16(3), 224-231 (2000)
Xiaomin Huang et al.
Cell death & disease, 15(4), 258-258 (2024-04-13)
The impairment of the blood-brain barrier (BBB) has been increasingly recognised as a critical element in the early pathogenesis of Alzheimer's disease (AD), prompting a focus on brain endothelial cells (BECs), which serve as the primary constituents of the BBB.
Chiara Levra Levron et al.
Nature cell biology, 25(5), 740-753 (2023-04-21)
Epithelial cells that participated in wound repair elicit a more efficient response to future injuries, which is believed to be locally restricted. Here we show that cell adaptation resulting from a localized tissue damage has a wide spatial impact at
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