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Key Documents

HPA031345

Sigma-Aldrich

Anti-SLC2A1 antibody produced in rabbit

enhanced validation

affinity isolated antibody, buffered aqueous glycerol solution

Synonyme(s) :

Anti-DYT18, Anti-GLUT, Anti-GLUT1, Anti-HTLVR

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About This Item

Code UNSPSC :
12352203
Numéro HPA (Human Protein Atlas):
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous glycerol solution

Espèces réactives

human

Validation améliorée

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

Technique(s)

immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:1000-1:2500

Séquence immunogène

GRTFDEIASGFRQGGASQSDKTPEELFHP

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... SLC2A1(6513)

Description générale

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.

Immunogène

solute carrier family 2 (facilitated glucose transporter), member 1

Application

Anti-SLC2A1 antibody produced in rabbit has been used in immunohistochemistry.

Actions biochimiques/physiologiques

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.

Caractéristiques et avantages

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:
  • 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.

Liaison

Corresponding Antigen APREST87043

Forme physique

Solution in phosphate buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide.

Informations légales

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

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
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
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.
Mutational analysis of GLUT1 (SLC2A1) in Glut-1 deficiency syndrome.
Wang D, et al.
Human Genetics, 16(3), 224-231 (2000)
FZD10-Gα13 signalling axis points to a role of FZD10 in CNS angiogenesis.
Hot B, et al.
Cellular Signalling, 32, 93-103 (2017)

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