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Noun1.cyclooxygenase-1 - an enzyme that regulates prostaglandins that are important for the health of the stomach lining and kidneys; "an unfortunate side effect of NSAIDs is that they block Cox-1"
Cox, cyclooxygenase - either of two related enzymes that control the production of prostaglandins and are blocked by aspirin
References in periodicals archive ?
Ginger suppresses prostaglandin synthesis through inhibition of cyclooxygenase-1 and cyclooxygenase-2 thereby its usefulness in arthritis was understood.
Crypt stem cell survival in the mouse intestinal epithelium is regulated by prostaglandins synthesized through cyclooxygenase-1.
Cyclooxygenase-1 and cyclooxygenase-2 selectivity of widely used nonsteroidal anti-inflammatory drugs.
Identification and functional analysis of cyclooxygenase-1 as a molecular target of boswellic acids.
Molecular identification of cytosolic prostaglandin E2 synthase that is functionally coupled with cyclooxygenase-1 in immediate prostaglandin E2 biosynthesis.
If they ingest a cyclooxygenase-1 inhibitor, they develop asthma symptoms, rhinorrhea, periorbital edema, urticaria, pruritus, angioedema, anaphylaxis, or other symptoms.
However, it appears to boost production of cyclooxygenase-1 (COX-1), a protein that boosts kidney function, the researchers said.
A second key finding of his study of aspirin resistance in 120 patients with stable CAD, including 30 with diabetes, was that not all of aspirin's antiplatelet effects in diabetic patients were mediated by inhibition of cyclooxygenase-1, the pathway previously believed to be solely responsible for the drug's antithrombotic efficacy.
As can be seen in Figure 3, both cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2) also participate in the degradation of arachidonic acid.
COX-3: A splice variant of cyclooxygenase-1 in mouse neural tissue and cells.
Because both aspirin and NSAIDs inhibit the action of the isoenzyme cyclooxygenase-1 (COX-1), the researchers performed a subanalysis of the aspirin component of the study to examine the extent to which regular NSAID use blocked the benefits of aspirin.

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