Render Target: STATIC
Render Timestamp: 2024-12-02T11:08:57.731Z
Commit: cd2fae6ca3f811b1ddb1df24ac291ed56d5d501b
XML generation date: 2024-09-30 01:55:30.303
Product last modified at: 2024-11-14T13:15:23.499Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

FTO (D2V1I) Rabbit mAb #45980

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 60
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    FTO (D2V1I) Rabbit mAb recognizes endogenous levels of total FTO protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly87 of human FTO protein.

    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).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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