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Render Timestamp: 2024-11-21T14:08:12.416Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:58:31.016
Product last modified at: 2024-09-30T08:00:28.615Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
  1. Products /
  2. Primary Antibodies /
  3. SOAT1 (E5O4K) Rabbit mAb
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

SOAT1 (E5O4K) Rabbit mAb #84476

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 45
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200

    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

    SOAT1 (E5O4K) Rabbit mAb recognizes endogenous levels of total SOAT1 protein. The higher molecular weight bands observed at 90 kDa, 135 kDa, and 185 kDa in the IP experiment are probably due to the oligomer formation under the IP lysate condition.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human SOAT1 protein.

    Background

    SOAT1 (Sterol O-acyltransferase 1; ACAT1) is an O-acyltransferase that functions in the endoplasmic reticulum (ER) to catalyze the formation of cholesterol esters from free cholesterol and long chain fatty acyl-coenzyme A. The cholesterol esters are incorporated into cytoplasmic lipid droplets, thereby preventing excess free cholesterol from inducing lipid-mediated cell toxicity, including ER stress (1). Research studies have shown that pharmacological inhibition of SOAT1 in tumor cells induced lipid-mediated cell toxicity that suppressed tumor cell growth and promoted tumor cell apoptosis (2,3). Pharmacological SOAT1 inhibition was also shown to stimulate autophagy-mediated proteolysis in microglia, leading to enhanced clearance of amyloid peptide Aβ42 (4,5). Collectively, these findings suggest that SOAT1 inhibition may have therapeutic potential in both cancer and Alzheimer’s disease.

    Database Links

    UniProt ID: P35610


    Entrez-Gene Id: 6646


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