Render Target: STATIC
Render Timestamp: 2024-10-25T10:24:04.927Z
Commit: 56767fe525c928647c8401233a175d0d607d385d
XML generation date: 2024-09-30 01:55:12.591
Product last modified at: 2024-10-10T14:15:15.082Z
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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.

FAAH1 (C84F1) Rabbit mAb #3829

Filter:
  • WB
  • IP
  • IHC

    Supporting Data

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

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunohistochemistry (Paraffin) 1:3200 - 1:12800

    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

    FAAH1 (C84F1) Rabbit mAb detects endogenous levels of total FAAH1 protein.

    Species Reactivity:

    Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues from the sequence of human FAAH1 protein.

    Background

    Endogenous cannabinoids have been implicated in addictive behaviors and drug abuse (1). Fatty-acid amide hydrolase 1 (FAAH1) is a plasma membrane-bound hydrolase that converts oleamide to oleic acid (2). This hydrolase also converts the cannabinoid anandamide, the endogenous ligand for the CB1 cannabinoid receptor, to arachidonic acid, suggesting a role in fatty-acid amide inactivation (2). Mice lacking FAAH1 have significantly higher levels of anandamide in the brain and show decreased sensitivity to pain, further indicating a role for FAAH1 in the regulation of endocannabinoid signaling in vivo (3). FAAH1 null mice also demonstrate an increased preference for alcohol and an increased voluntary uptake of alcohol as compared to wild-type mice, indicating a role of FAAH1 in modulating addictive behaviors (1).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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    U.S. Patent No. 7,429,487, foreign equivalents, and child patents deriving therefrom.
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