FTO Antibody #14386
- WB
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 60 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
FTO Antibody recognizes endogenous levels of total FTO protein.
Species Reactivity:
Human
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu464 of human FTO protein. Antibodies are purified by protein A and peptide affinity chromatography.
Background
FTO (fat mass and obesity-associated protein) is the first obesity gene product identified by genome-wide association studies and it is associated with the largest effect size for this class of proteins (1-4). Multiple single-nucleotide polymorphisms (SNPs) in the first intron of the FTO gene have been associated with increased body weight and obesity. Further studies reported that FTO risk alleles were associated with an increase in energy intake, a reduction of activity, and possibly an increased daily fat intake (4).
FTO is a DNA and RNA demethylase that catalyzes the oxidative demethylation of thymidine and uracil. Among its targets is an mRNA subset involved in regulation of learning, reward behavior, motor functions, and feeding (5). Loss of the FTO gene in mice leads to postnatal growth retardation and a significant reduction in adipose tissue. Mice deficient in the FTO gene have lean body mass due to increased energy expenditure and systemic activation of sympathetic neurons, while overexpression of FTO in mice leads to increased food intake and results in obesity. These results demonstrate that FTO is functionally involved in energy homeostasis (6-8).
- Frayling, T.M. et al. (2007) Science 316, 889-94.
- Scuteri, A. et al. (2007) PLoS Genet 3, e115.
- Dina, C. et al. (2007) Nat Genet 39, 724-6.
- Gulati, P. and Yeo, G.S. (2013) Diabetologia 56, 2113-21.
- Hess, M.E. et al. (2013) Nat Neurosci 16, 1042-8.
- Fischer, J. et al. (2009) Nature 458, 894-8.
- Tews, D. et al. (2013) Endocrinology 154, 3141-51.
- Church, C. et al. (2010) Nat Genet 42, 1086-92.
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