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Merck
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安全信息

HPA023296

Sigma-Aldrich

Anti-ALDH7A1 antibody produced in rabbit

enhanced validation

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

别名:

Anti-Aldehyde dehydrogenase family 7 member A1, Anti-Alpha-AASA dehydrogenase, Anti-Alpha-aminoadipic semialdehyde dehydrogenase, Anti-Antiquitin-1, Anti-Delta1-piperideine-6-carboxylate dehydrogenease, Anti-P6c dehydrogenase

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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

产品线

Prestige Antibodies® Powered by Atlas Antibodies

形式

buffered aqueous glycerol solution

种属反应性

human

增强验证

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

技术

immunoblotting: 0.04-0.4 μg/mL
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:1000-1:2500

免疫原序列

DLSLVVPSALFAAVGTAGQRCTTARRLFIHESIHDEVVNRLKKAYAQIRVGNPWDPNVLYGPLHTKQAVSMFLGAVEEAKKEGGTVVYGGKVMDRPGNYVEPTIVTGLGHDASIAHTETFAPILY

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 ... ALDH7A1(501)

一般描述

The gene ALDH7A1 (aldehyde dehydrogenase 7 family member A1) is mapped to human chromosome 5q31. It is present in the cytoplasm and mitochondria.

免疫原

Alpha-aminoadipic semialdehyde dehydrogenase recombinant protein epitope signature tag (PrEST)

应用

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.

生化/生理作用

ALDH7A1 (aldehyde dehydrogenase 7 family member A1) is needed for lysine catabolism. It is responsible for NAD+ (nicotinamide adenine dinucleotide)-dependent oxidation of α-aminoadipate semialdehyde (AASA) to α-aminoadipate (AA). It is also required for the degradation of acetaldehyde which is made during alcohol metabolism. It is upregulated in various cancers, including prostate cancer, non-small cell lung carcinoma and ovarian tumors. Mutations in ALDH7A1 are linked with seizure disorder pyridoxine-dependent epilepsy (PDE).

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 APREST75498

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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WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

常规特殊物品

分析证书(COA)

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Diana Andrejeva et al.
BMC cancer, 18(1), 1180-1180 (2018-11-30)
Changes in cellular metabolism are now recognized as potential drivers of cancer development, rather than as secondary consequences of disease. Here, we explore the mechanism by which metabolic changes dependent on aldehyde dehydrogenase impact cancer development. ALDH7A1 was identified as
Haiyong Wang et al.
Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 35(12), 12665-12670 (2014-09-13)
Although the entire etiology of esophageal squamous cell carcinoma (ESCC) is still unclear, alcohol drinking has been identified as a major environmental risk factor. The aldehyde dehydrogenase (ALDH) superfamily members are major enzymes involved in the alcohol-metabolizing pathways. Accumulating evidences
Min Luo et al.
Biochemistry, 54(35), 5513-5522 (2015-08-12)
Aldehyde dehydrogenase 7A1 (ALDH7A1) is part of lysine catabolism and catalyzes the NAD(+)-dependent oxidation of α-aminoadipate semialdehyde to α-aminoadipate. Herein, we describe a structural study of human ALDH7A1 focused on substrate recognition. Five crystal structures and small-angle X-ray scattering data
Laura A Jansen et al.
Annals of neurology, 75(1), 22-32 (2013-10-15)
A high incidence of structural brain abnormalities has been reported in individuals with pyridoxine-dependent epilepsy (PDE). PDE is caused by mutations in ALDH7A1, also known as antiquitin. How antiquitin dysfunction leads to cerebral dysgenesis is unknown. In this study, we
Zhixian Yang et al.
PloS one, 9(3), e92803-e92803 (2014-03-26)
Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive disorder that causes seizures in neonates and infants. Mutations of the ALDH7A1 gene are now recognized as the molecular basis PDE and help to define this disease. Three Chinese children with PDE

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