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HPA006308

Sigma-Aldrich

Anti-DDAH1 antibody produced in rabbit

enhanced validation

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

Synonyme(s) :

Anti-DDAH-1, Anti-DDAHI, Anti-Dimethylargininase-1, Anti-Dimethylarginine dimethylaminohydrolase 1, Anti-N recombinant

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About This Item

Code UNSPSC :
12352203
Numéro HPA (Human Protein Atlas):
Nomenclature NACRES :
NA.43

Source biologique

rabbit

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

mouse, human, rat

Validation améliorée

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

Technique(s)

immunoblotting: 0.04-0.4 μg/mL
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:500-1:1000

Séquence immunogène

SKRTNQRGAEILADTFKDYAVSTVPVADGLHLKSFCSMAGPNLIAIGSSESAQKALKIMQQMSDHRYDKLTVPDDIAANCIYLNIPNKGHVLLHRTPEEYPESAKVYEKLKDHMLIPVSMSELEKVDGLLT

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 ... DDAH1(23576)

Immunogène

N recombinant protein epitope signature tag (PrEST)

Application

Anti-DDAH1 antibody produced in rabbit, a Prestige Antibody, is developed and validated by the Human Protein Atlas (HPA) project . Each antibody is tested by immunohistochemistry against hundreds of normal and disease tissues. These images can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. The antibodies are also tested using immunofluorescence and western blotting. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.

Actions biochimiques/physiologiques

Dimethylarginine dimethylaminohydrolases 1 (DDAH1) is one of the key enzymes involved in the inactivation of asymmetric dimethylarginine (ADMA). This enzyme is primarily responsible for ADMA metabolism. Varaints of this gene is linked with serum ADMA levels in type 2 diabetes (T2DM). It might also have an affect on the ADMA levels in the serum in individuals with T1DM.

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 APREST70256

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

Tao Sun et al.
American journal of hypertension, 26(12), 1437-1444 (2013-07-19)
Dimethylarginine dimethylaminohydrolases 1 (DDAH1) is the major enzyme responsible for inactivation of asymmetric dimethylarginine (ADMA). This study seeks to clarify the correlations between mRNA expression levels of DDAH1 transcript variants and the relationship with ADMA metabolizing activity in human. The
Alena A Kozlova et al.
Cellular and molecular neurobiology (2021-05-21)
The endogenous methylated derivative of ʟ-arginine, Nω,Nω'-dimethyl-ʟ-arginine (asymmetric dimethylarginine, ADMA), an independent risk factor in many diseases, inhibits the activity of nitric oxide synthases and, consequently, modulates the availability of nitric oxide. While most studies on the biological role of
Rhys D Fogarty et al.
Journal of diabetes and its complications, 26(3), 195-198 (2012-04-24)
Asymmetric dimethylarginine (ADMA) levels are elevated in diabetes and likely contribute to diabetic complications such as retinopathy and nephropathy. The DDAH enzymes are primarily responsible for ADMA metabolism. Polymorphisms in the dimethylarginine dimethylaminohydrolase (DDAH) 1 and 2 genes have been
Alena A Kozlova et al.
Journal of neural transmission (Vienna, Austria : 1996) (2023-02-16)
The enzyme dimethylarginine dimethylaminohydrolase 1 (DDAH1) plays a pivotal role in the regulation of nitric oxide levels by degrading the main endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA). Growing evidence highlight the potential implication of DDAH/ADMA axis in the
Zhili Shao et al.
Journal of the American College of Cardiology, 59(13), 1150-1158 (2012-03-24)
This study sought to examine the hemodynamic determinants of dysregulated arginine metabolism in patients with acute decompensated heart failure and to explore possible mechanisms of arginine dysregulation in human heart failure. Accumulating methylated arginine metabolites and impaired arginine bioavailability have

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