产品名称
Anti-FLAD1 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution, ab3
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
human
technique(s)
immunohistochemistry: 1:20- 1:50
immunogen sequence
RTDPYSCSLCPFSPTDPGWPAFMRINPLLDWTYRDIWDFLRQLFVPYCILYDRGYTSLGSRENTVRNPALKCLSPGGHPTYRPAYLLENEE
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... FLAD1(80308)
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.
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.
Anti-FLAD1 antibody has been used in immunoblotting.
Biochem/physiol Actions
FAD synthase (FADS) may participate in human metabolism. It catalyzes the production of FAD from FMN. FADS enzyme coded by FLAD1 helps in the conversion of riboflavin into the redox cofactor FAD.
Disclaimer
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.
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.
General description
FLAD1(flavin adenine dinucleotide synthetase 1) codes for FAD synthase (FADS) enzyme. It is an important enzyme in the metabolic pathway and has MPTb (molybdopterin binding) and FADS domains. This gene is located on human chromosome 1q21.3.
Immunogen
FAD1 flavin adenine dinucleotide synthetase homolog (S. cerevisiae) recombinant protein epitope signature tag (PrEST)
Other Notes
Corresponding Antigen APREST76940
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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存储类别
10 - Combustible liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Riboflavin-responsive and-non-responsive mutations in FAD synthase cause multiple acyl-CoA dehydrogenase and combined respiratory-chain deficiency.
Olsen RK, et al.
American Journal of Human Genetics, 98(6), 1130-1145 (2016)
B Ryder et al.
JIMD reports, 45, 37-44 (2018-10-13)
Multiple acyl-CoA dehydrogenase deficiency (MADD) or glutaric aciduria type II (GAII) is a clinically heterogeneous disorder affecting fatty acid and amino acid metabolism. Presentations range from a severe neonatal form with hypoglycemia, metabolic acidosis, and hepatomegaly with or without congenital
Over-expression in Escherichia coli and characterization of two recombinant isoforms of human FAD synthetase.
Brizio C, et al.
Biochemical and Biophysical Research Communications, 344(3), 1008-1016 (2006)
Rikke K J Olsen et al.
American journal of human genetics, 98(6), 1130-1145 (2016-06-04)
Multiple acyl-CoA dehydrogenase deficiencies (MADDs) are a heterogeneous group of metabolic disorders with combined respiratory-chain deficiency and a neuromuscular phenotype. Despite recent advances in understanding the genetic basis of MADD, a number of cases remain unexplained. Here, we report clinically
Kai Muru et al.
Molecular genetics & genomic medicine, 7(9), e915-e915 (2019-08-09)
Multiple acyl-CoA dehydrogenase deficiency (MADD), also known as glutaric aciduria type II, is a mitochondrial fatty acid oxidation disorder caused by variants in ETFA, ETFB, and ETFDH. Recently, riboflavin transporter genes and the mitochondrial FAD transporter gene have also been
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