Render Target: STATIC
Render Timestamp: 2024-11-05T11:14:09.517Z
Commit: 57f6e368eba1a427377652f2ad915d45d7f340a4
XML generation date: 2024-10-21 16:05:53.117
Product last modified at: 2024-10-31T20:45:09.104Z
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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.

CPT1A (E3Y1V) Rabbit mAb #97361

Filter:
  • WB
  • IP
  • IHC
  • IF
  • F

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 88
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunohistochemistry (Paraffin) 1:100 - 1:400
    Immunofluorescence (Immunocytochemistry) 1:400 - 1:1600
    Flow Cytometry (Fixed/Permeabilized) 1:200 - 1:800

    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

    CPT1A (E3Y1V) Rabbit mAb recognizes endogenous levels of total CPT1A protein. This antibody does not cross-react with CPT1B, CPT1C, or CPT2.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu696 of human CPT1A protein.

    Background

    Carnitine palmitoyltransferase-1 (CPT1), localized to the mitochondrial outer membrane, translocates fatty acids across the mitochondrial membranes and catalyzes the rate-limiting step of β-oxidation (1,2). There are three isoforms of this enzyme: CPT1A (liver), CPT1B (muscle), and CPT1C (brain) (1,2). Deficiency of CPT1A results in an autosomal recessive mitochondrial fatty acid oxidation disorder (3). Studies have shown that physiological high blood glucose and insulin levels inhibit CPT1B activity in human muscle and therefore divert long-chain fatty acids toward storage in human muscle as triglycerides (4). Furthermore, mice deficient in CPT1C show less food intake and reduced body weight (5). These findings suggest that CPT1 may play a role in metabolic syndromes.
    For Research Use Only. Not For Use In Diagnostic Procedures.
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