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HPA018921

Sigma-Aldrich

Anti-ETFB antibody produced in rabbit

enhanced validation

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution, Ab2

Synonym(s):

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

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About This Item

UNSPSC Code:
12352203
Human Protein Atlas Number:
NACRES:
NA.43

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

product line

Prestige Antibodies® Powered by Atlas Antibodies

form

buffered aqueous glycerol solution

species reactivity

mouse, human, rat

enhanced validation

independent
Learn more about Antibody Enhanced Validation

technique(s)

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

immunogen sequence

ETIRTALAMGADRGIHVEVPPAEAERLGPLQVARVLAKLAEKEKVDLVLLGKQAIDDDCNQTGQMTAGFLDWPQGTFASQVTLEGDKLKVEREID

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ETFB(2109)

General description

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)

Application

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 Actions

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).

Features and Benefits

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.

Linkage

Corresponding Antigen APREST74685

Physical form

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

Legal Information

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

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Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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)
D L Roberts et al.
Proceedings of the National Academy of Sciences of the United States of America, 93(25), 14355-14360 (1996-12-10)
Mammalian electron transfer flavoproteins (ETF) are heterodimers containing a single equivalent of flavin adenine dinucleotide (FAD). They function as electron shuttles between primary flavoprotein dehydrogenases involved in mitochondrial fatty acid and amino acid catabolism and the membrane-bound electron transfer flavoprotein
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
Manuel Schiff et al.
Molecular genetics and metabolism, 88(2), 153-158 (2006-03-03)
Multiple acyl-CoA dehydrogenase deficiency (MADD) is a recessively inherited metabolic disorder that can be due to a deficiency of electron transfer flavoprotein (ETF) or its dehydrogenase (ETF-ubiquinone oxidoreductase). ETF is a mitochondrial matrix protein consisting of alpha- (30kDa) and beta-

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