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5743 19225 Ensembl ENSG00000073756 ENSMUSG00000032487 UniProt P35354 Q05769 RefSeq (mRNA) NM_000963 NM_011198 RefSeq (protein) NP_000954 NP_035328 Location (UCSC) Chr 1: 186.67 – 186.68 Mb Chr 1: 149.98 – 149.98 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Cyclooxygenase-2 (COX-2), also known as prostaglandin-endoperoxide synthase 2 (HUGO PTGS2), is an enzyme that in humans is ...
Cyclooxygenase (COX), officially known as prostaglandin-endoperoxide synthase (PTGS), is an enzyme (specifically, a family of isozymes, EC 1.14.99.1) that is responsible for biosynthesis of prostanoids, including thromboxane and prostaglandins such as prostacyclin, from arachidonic acid.
In 1991 the existence of the COX-2 enzyme was confirmed by being cloned by Dr. Dan Simmons at Brigham Young University. Before the confirmation of COX-2 existence, the Dupont company had developed a compound, DuP-697, that was potent in many anti-inflammatory assays but did not have the ulcerogenic effects of NSAIDs. Once the COX-2 enzyme was ...
Prostaglandins are produced following the sequential oxygenation of arachidonic acid, DGLA or EPA by cyclooxygenases (COX-1 and COX-2) and terminal prostaglandin synthases. The classic dogma is as follows: COX-1 is responsible for the baseline levels of prostaglandins. COX-2 produces prostaglandins through stimulation.
The underlying mechanism for the deleterious effect proposes that endothelial cells lining the microvasculature in the body express COX-2, whose selective inhibition results in levels of prostaglandin I2 (PGI2, prostacyclin) down-regulated relative to thromboxane (since COX-1 in platelets is unaffected).
Then TXA 2 mediates the release of the vasodilators PGE 2 and LTB 4. The blood vessels engorge and the injury reddens. Swelling—LTB 4 makes the blood vessels more permeable. Plasma leaks out into the connective tissues, and they swell. The process also loses pro-inflammatory cytokines. Pain—The cytokines increase COX-2 activity.
The MT-CO2 gene produces a 25.6 kDa protein composed of 227 amino acids. [6] [7] MT-CO2 is a subunit of the enzyme Cytochrome c oxidase (EC 1.9.3.1) [8] [9] (Complex IV), an oligomeric enzymatic complex of the mitochondrial respiratory chain involved in the transfer of electrons from cytochrome c to oxygen.
The inhibition of COX-2 is paramount for the anti-inflammatory and analgesic function of the selective COX-2 inhibitor celecoxib. However, with regard to this drug's promise for the therapy of advanced cancers, it is unclear whether the inhibition of COX-2 plays a dominant role, and this has become a controversial and intensely researched issue.