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Merck

HPA039017

Sigma-Aldrich

Anti-MMAB antibody produced in rabbit

enhanced validation

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

Synonym(e):

Anti-CFAP23, Anti-cblB

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About This Item

UNSPSC-Code:
12352203
Human Protein Atlas-Nummer:
NACRES:
NA.41

Biologische Quelle

rabbit

Konjugat

unconjugated

Antikörperform

affinity isolated antibody

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Produktlinie

Prestige Antibodies® Powered by Atlas Antibodies

Form

buffered aqueous glycerol solution

Speziesreaktivität

human

Erweiterte Validierung

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

Methode(n)

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

Immunogene Sequenz

AFILPSGGKISSALHFCRAVCRRAERRVVPLVQMGETDANVAKFLNRLSDYLFTLARYAAMKEGNQEKIYMKNDPSAESEGL

UniProt-Hinterlegungsnummer

Versandbedingung

wet ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... MMAB(326625)

Allgemeine Beschreibung

Methylmalonic aciduria cblB type (MMAB) gene, spanning 19.8kb length with 9 exons, is mapped to human chromosome 12q24.11. The gene codes for a 27.4kDa ATP cob (I) alamin adenosyltransferase (ATR) protein composed of 250 amino acids. The protein belongs to the family of PduO family of cobalamin adenosyltransferase.

Immunogen

methylmalonic aciduria (cobalamin deficiency) cblB type recombinant protein epitope signature tag (PrEST)

Anwendung

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.

Biochem./physiol. Wirkung

ATP cob (I) alamin adenosyltransferase (ATR) /methylmalonic aciduria cblB type (MMAB) is a novel mitochondrial enzyme involved in the vitamin B12 metabolism. It catalyzes the conversion of reduced cob (I) alamin to the adenosylcobalamin cofactor. Genetic variation of the gene is associated with the cblB type methylmalonic aciduria. In addition, polymorphism in MMAB gene is associated with the increased plasma high-density lipoprotein cholesterol (HDL-C) levels and decreased risk of coronary heart disease (CHD) in Chinese population.

Leistungsmerkmale und Vorteile

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.

Verlinkung

Corresponding Antigen APREST81082

Physikalische Form

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

Rechtliche Hinweise

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

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 1

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

Besitzen Sie dieses Produkt bereits?

In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.

Die Dokumentenbibliothek aufrufen

Functional and structural analysis of five mutations identified in methylmalonic aciduria cblB type.
Jorge-Finnigan A
Human Mutation, 31, 1033-1042 (2010)
Advances in the understanding of cobalamin assimilation and metabolism.
Quadros EV
British Journal of Haematology, 148, 195-204 (2010)
Patrick Forny et al.
Human genetics (2021-11-20)
Pathogenic variants in MMAB cause cblB-type methylmalonic aciduria, an autosomal-recessive disorder of propionate metabolism. MMAB encodes ATP:cobalamin adenosyltransferase, using ATP and cob(I)alamin to create 5'-deoxyadenosylcobalamin (AdoCbl), the cofactor of methylmalonyl-CoA mutase (MMUT). We identified bi-allelic disease-causing variants in MMAB in
Association of KCTD10, MVK, and MMAB polymorphisms with dyslipidemia and coronary heart disease in Han Chinese population.
Sun J
Lipids in Health and Disease, 15, 171-171 (2016)
Ligand-binding by catalytically inactive mutants of the cblB complementation group defective in human ATP:cob(I)alamin adenosyltransferase.
Zhang J
Molecular Genetics and Metabolism, 98, 278-284 (2009)

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