HPA018993
Anti-ETFA antibody produced in rabbit
Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Synonym(s):
Anti-Alpha-ETF, Anti-Electron transfer flavoprotein subunit alpha, mitochondrial precursor
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About This Item
biological source
rabbit
Quality Level
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
human
enhanced validation
orthogonal RNAseq
independent
Learn more about Antibody Enhanced Validation
technique(s)
immunoblotting: 0.04-0.4 μg/mL
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:50-1:200
immunogen sequence
MFRAAAPGQLRRAASLLRFQSTLVIAEHANDSLAPITLNTITAATRLGGEVSCLVAGTKCDKVAQDLCKVAGIAKVLVAQHDVYKGL
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... ETFA(2108)
Related Categories
General description
The gene electron transfer flavoprotein subunit α (ETFA) is mapped to human chromosome 15q23. The protein localizes in the mitochondria.
Immunogen
Electron transfer flavoprotein subunit alpha, mitochondrial precursor recombinant protein epitope signature tag (PrEST)
Application
Anti-ETFA 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.
Biochem/physiol Actions
ETFA (electron transfer flavoprotein subunit α) 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 ETFA 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:
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 APREST74743
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
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
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Y Indo et al.
American journal of human genetics, 49(3), 575-580 (1991-09-01)
In our previous study of eight glutaric acidemia type II (GAII) fibroblast lines by using [35S]methionine labeling and immunoprecipitation, three of them had a defect in the synthesis of the alpha-subunit of electron transfer flavoprotein (alpha-ETF) (Ikeda et al. 1986).
Ronald J A Wanders et al.
Journal of inherited metabolic disease, 33(5), 479-494 (2010-05-22)
Oxidation of fatty acids in mitochondria is a key physiological process in higher eukaryotes including humans. The importance of the mitochondrial beta-oxidation system in humans is exemplified by the existence of a group of genetic diseases in man caused by
Erik Björling et al.
Molecular & cellular proteomics : MCP, 7(10), 2028-2037 (2008-08-01)
Antibodies are useful tools to characterize the components of the human proteome and to validate potential protein biomarkers discovered through various clinical proteomics efforts. The lack of validation results across various applications for most antibodies often makes it necessary to
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-
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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