Anti-COX2 / Cyclooxygenase 2 Rabbit mAb

Primary Antibodies

COX2 / Cyclooxygenase 2

Store at -20°C. Avoid freeze/thaw cycles.

Cyclooxygenase1 (Cox1) and cyclooxygenase2 (Cox2), family members with 60% homology in humans, catalyze prostaglandin production from arachidonic acid. While Cox1 expression is constitutive in most tissues, Cox2 expression is induced by lipopolysaccharide (LPS) and peptidoglycan (PGN). 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. Investigators have shown that LPS and PGN induce the clinical manifestations of arthritis and bacterial infections, such as inflammation, fever, and septic shock. 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.

PBS

Recombinant Monoclonal

Cyclooxygenase1 (Cox1) and cyclooxygenase2 (Cox2), family members with 60% homology in humans, catalyze prostaglandin production from arachidonic acid. While Cox1 expression is constitutive in most tissues, Cox2 expression is induced by lipopolysaccharide (LPS) and peptidoglycan (PGN). 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. Investigators have shown that LPS and PGN induce the clinical manifestations of arthritis and bacterial infections, such as inflammation, fever, and septic shock. 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.