Render Target: STATIC
Render Timestamp: 2024-12-26T11:26:47.004Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-12-13 16:01:07.784
Product last modified at: 2024-12-14T08:01:00.854Z
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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.

Cox2 (F1F3H) Rabbit mAb #43542

Filter:
  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa) 74
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Simple Western™ 1:10 - 1:50
    Immunoprecipitation 1:50
    Immunofluorescence (Immunocytochemistry) 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

    Cox2 (F1F3H) Rabbit mAb recognizes endogenous levels of total Cox2 protein. Reactivity by immunofluorescence is human only.

    Species Reactivity:

    Human, Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human Cox2 protein.

    Background

    Cyclooxygenase1 (Cox1) and cyclooxygenase2 (Cox2), family members with 60% homology in humans, catalyze prostaglandin production from arachidonic acid (1,2). While Cox1 expression is constitutive in most tissues, Cox2 expression is induced by lipopolysaccharide (LPS) and peptidoglycan (PGN) (3). PGN activates Ras, leading to phosphorylation of Raf at Ser338 and Erk1/2 at Tyr204. The activation of MAP kinase signaling results in subsequent activation of IKKα/β, phosphorylation of IκBα at Ser32/36, and NF-κB activation. Finally, activation of the transcription factor NF-κB is responsible for the induction of Cox2 expression (4). Investigators have shown that LPS and PGN induce the clinical manifestations of arthritis and bacterial infections, such as inflammation, fever, and septic shock (5). Research studies have indicated that Cox1 and Cox2 may also play a role in the neuropathology of Alzheimer's disease by potentiating γ-secretase activity and β-amyloid generation (6).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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