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Key Documents

HPA016646

Sigma-Aldrich

Anti-ASL antibody produced in rabbit

enhanced validation

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

Synonyme(s) :

Anti-ASAL, Anti-Argininosuccinate lyase, Anti-Arginosuccinase

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About This Item

Code UNSPSC :
12352203
Numéro HPA (Human Protein Atlas):

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Gamme de produits

Prestige Antibodies® Powered by Atlas Antibodies

Forme

buffered aqueous glycerol solution

Espèces réactives

human

Validation améliorée

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

Technique(s)

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

Séquence immunogène

MASESGKLWGGRFVGAVDPIMEKFNASIAYDRHLWEVDVQGSKAYSRGLEKAGLLTKAEMDQILHGLDKVAEEWAQGTFKLNSNDED

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 ... ASL(435)

Description générale

ASL (Argininosuccinate lyase) exists in monomeric state with ~52kDa molecular weight. It turns into the homotetrameric functional state after addition of four active sites. It is highly expressed in liver but also found at low extent in kidney, small intestine, pancreas, muscle, brain, heart, and erythroblast.

Immunogène

Argininosuccinate lyase recombinant protein epitope signature tag (PrEST)

Application

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)

Actions biochimiques/physiologiques

ASL (Argininosuccinate lyase) plays a vital role in hepatic urea cycle. It stimulates the conversion of argininosuccinate into arginine and fumarate. This hydrolytic separation helps to remove waste nitrogen. It also produces nitric oxide through the arginine-citrulline cycle. Mutation in ASL gene causes an autosomal recessive disorder, argininosuccinic aciduria. Study has been reported that ASL behaves as a prognostic marker in several types of hepatocellular carcinomas (HCC).

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 APREST74654

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

Équipement de protection individuelle

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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

Scott N Ashley et al.
Molecular genetics and metabolism, 125(3), 241-250 (2018-09-27)
Argininosuccinic aciduria (ASA) is the second most common genetic disorder affecting the urea cycle. The disease is caused by deleterious mutations in the gene encoding argininosuccinate lyase (ASL); total loss of ASL activity results in severe neonatal onset of the
Anke Werner et al.
Frontiers in immunology, 8, 864-864 (2017-08-10)
In the tumor microenvironment, arginine is metabolized by arginase-expressing myeloid cells. This arginine depletion profoundly inhibits T cell functions and is crucially involved in tumor-induced immunosuppression. Reconstitution of adaptive immune functions in the context of arginase-mediated tumor immune escape is
Margaret P Adam et al.
GeneReviews(?), 2011 3 (Updated 2012 2) (2012-02-02)
Deficiency of argininosuccinate lyase (ASL), the enzyme that cleaves argininosuccinic acid to produce arginine and fumarate in the fourth step of the urea cycle, is characterized by a severe neonatal onset form and a late onset form. The severe neonatal
Hua Yang et al.
Applied immunohistochemistry & molecular morphology : AIMM, 20(6), 602-606 (2012-04-26)
Argininosuccinate lyase (ASL) is an important enzyme in the hepatic urea cycle, and catalyzes the reversible reaction of argininosuccinate to arginine and fumarate. Its expression is significantly reduced in some hepatocellular carcinomas (HCC). In this study, we aimed to investigate
Liyan Hu et al.
The Journal of biological chemistry, 288(48), 34599-34611 (2013-10-19)
Argininosuccinic aciduria (ASA) is an autosomal recessive urea cycle disorder caused by deficiency of argininosuccinate lyase (ASL) with a wide clinical spectrum from asymptomatic to severe hyperammonemic neonatal onset life-threatening courses. We investigated the role of ASL transcript variants in

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