Title : COX-2 is not involved in thromboxane biosynthesis by activated human platelets.

Pub. Date : 1999 Dec

PMID : 10639016






6 Functional Relationships(s)
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1 Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance. Aspirin mitochondrially encoded cytochrome c oxidase II Homo sapiens
2 Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance. Aspirin mitochondrially encoded cytochrome c oxidase II Homo sapiens
3 Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance. Aspirin mitochondrially encoded cytochrome c oxidase II Homo sapiens
4 Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance. Aspirin mitochondrially encoded cytochrome c oxidase II Homo sapiens
5 However the cellular source(s) of COX-2 possibly responsible for aspirin resistance remains unknown. Aspirin mitochondrially encoded cytochrome c oxidase II Homo sapiens
6 Our results argue against the involvement of COX-2 in TX biosynthesis by activated platelets and consequently dispute platelet COX-2 expression as an important mechanism of aspirin resistance. Aspirin mitochondrially encoded cytochrome c oxidase II Homo sapiens