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Render Timestamp: 2024-07-26T09:54:00.013Z
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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.

HMGCS2 (D3U1A) Rabbit mAb #20940

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 50
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    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

    HMGCS2 (D3U1A) Rabbit mAb recognizes endogenous levels of total HMGCS2 protein. This antibody does not cross-react with HMGCS1 protein.


    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro478 of human HMGCS2 protein.

    Background

    Mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (HMGCS2) generates hydroxymethylglutaryl-CoA (HMG-CoA) from acetyl-CoA and acetoacetyl-CoA, a rate-limiting step in ketogenesis (1). Starvation or a high-fat and low-carbohydrate diet increases the levels of hepatic FGF21, which in turn up-regulates HMGCS2 expression (2). Furthermore, mTORC1 inhibition was shown to be required for the increase of HMGCS2 expression mediated by PPARα in response to fasting (3). In addition, studies on mice lacking HMGCS2 suggest that ketogenesis plays a role in the prevention of diet-induced fatty liver injury and hyperglycemia (4).

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