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Merck
CN
所有图片(8)

主要文件

安全信息

HPA031345

Sigma-Aldrich

Anti-SLC2A1 antibody produced in rabbit

enhanced validation

affinity isolated antibody, buffered aqueous glycerol solution

别名:

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

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About This Item

UNSPSC代码:
12352203
人类蛋白质图谱编号:
NACRES:
NA.41

生物来源

rabbit

质量水平

偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

表单

buffered aqueous glycerol solution

种属反应性

human

增强验证

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

技术

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

免疫原序列

GRTFDEIASGFRQGGASQSDKTPEELFHP

UniProt登记号

运输

wet ice

储存温度

−20°C

靶向翻译后修饰

unmodified

基因信息

human ... SLC2A1(6513)

一般描述

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.

免疫原

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

应用

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

生化/生理作用

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.

特点和优势

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.

联系

Corresponding Antigen APREST87043

外形

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

法律信息

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

免责声明

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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储存分类代码

10 - Combustible liquids

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

常规特殊物品

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分析证书(COA)

Lot/Batch Number

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访问文档库

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.
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
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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