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Merck

HPA018923

Sigma-Aldrich

Anti-ETFB antibody produced in rabbit

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution, Ab3

Synonym(e):

Anti-Beta-ETF, Anti-Electron transfer flavoprotein subunit beta

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About This Item

UNSPSC-Code:
12352203
Human Protein Atlas-Nummer:

Biologische Quelle

rabbit

Qualitätsniveau

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

Methode(n)

immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:200-1:500

Immunogene Sequenz

GLALRPPPSCLFPPDPTPSPPAGQIRVKPDRTGVVTDGVKHSMNPFCEIAVEEAVRLKEKKLVKEVIAVSCGPAQCQ

UniProt-Hinterlegungsnummer

Versandbedingung

wet ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... ETFB(2109)

Allgemeine Beschreibung

The gene electron transfer flavoprotein subunit β (ETFB) is mapped to human chromosome 19q13.3. The protein localizes in the mitochondria.

Immunogen

Electron transfer flavoprotein subunit beta 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

ETFB (electron transfer flavoprotein subunit β) is a subunit of electron transfer flavoprotein (ETF). ETF is responsible for transfer of electrons from primary flavoprotein dehydrogenases participating in mitochondrial fatty acid and amino acid catabolism to the membrane-associated electron transfer flavoprotein ubiquinone oxidoreductase. Mutations in ETFB results in blockage of the electron transfer from acyl-CoA dehydrogenases. This results in accumulation of various acyl-esters in blood and urine causing multiple acyl-CoA dehydrogenation deficiency (MADD).

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 APREST74684

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

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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

Jędrzej Małecki et al.
The Journal of biological chemistry, 290(1), 423-434 (2014-11-25)
Proteins are frequently modified by post-translational methylation of lysine residues, catalyzed by S-adenosylmethionine-dependent lysine methyltransferases (KMTs). Lysine methylation of histone proteins has been extensively studied, but it has recently become evident that methylation of non-histone proteins is also abundant and
Bárbara J Henriques et al.
The Journal of biological chemistry, 284(7), 4222-4229 (2008-12-18)
Mutations in the genes encoding the alpha-subunit and beta-subunit of the mitochondrial electron transfer flavoprotein (ETF) and the electron transfer flavoprotein:ubiquinone oxidoreductase (ETF:QO) cause multiple acyl-CoA dehydrogenation deficiency (MADD), a disorder of fatty acid and amino acid metabolism. Point mutations
Assignment of the gene encoding the beta-subunit of the electron-transfer flavoprotein (ETFB) to human chromosome 19q13.3.
R Antonacci et al.
Genomics, 19(1), 177-179 (1994-01-01)
Shigenari Hirokawa et al.
Journal of dermatological science, 64(2), 119-126 (2011-09-10)
Fibroblast activation is strongly influenced by mechanical environment in the wound-healing process, especially in fibrosis. Mechanically stressed three-dimensional collagen embedded culture is a useful model representing fibroblasts in morphological as well as biochemical situations encountered during fibrosis. To find key
Rikke K J Olsen et al.
Human mutation, 22(1), 12-23 (2003-06-20)
Mutations in electron transfer flavoprotein (ETF) and its dehydrogenase (ETFDH) are the molecular basis of multiple acyl-CoA dehydrogenation deficiency (MADD), an autosomal recessively inherited and clinically heterogeneous disease that has been divided into three clinical forms: a neonatal-onset form with

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