Search results
Results from the WOW.Com Content Network
Cyclooxygenase-2 (COX-2), also known as prostaglandin-endoperoxide synthase 2 (HUGO PTGS2), is an enzyme that in humans is encoded by the PTGS2 gene. [5] In humans it is one of three cyclooxygenases. It is involved in the conversion of arachidonic acid to prostaglandin H 2, an important precursor of prostacyclin, which is expressed in inflammation.
COX is a common target for anti-inflammatory drugs. The most significant difference between the isoenzymes, which allows for selective inhibition, is the substitution of isoleucine at position 523 in COX-1 with valine in COX-2. The smaller Val 523 residue in COX-2 allows access to a hydrophobic side-pocket in the enzyme (which Ile 523 ...
Moreover, a recent study with various malignant tumor cells showed that celecoxib could inhibit the growth of these cells, even though some of these cancer cells didn't even contain COX-2. [ 20 ] Additional support for the idea that other targets besides COX-2 are important for celecoxib's anticancer effects has come from studies with ...
COX-2 produces prostaglandins through stimulation. However, while COX-1 and COX-2 are both located in the blood vessels, stomach and the kidneys, prostaglandin levels are increased by COX-2 in scenarios of inflammation and growth.
17709 Ensembl ENSG00000198712 ENSMUSG00000064354 UniProt P00403 P00405 RefSeq (mRNA) n/a n/a RefSeq (protein) n/a NP_904331 Location (UCSC) Chr M: 0.01 – 0.01 Mb Chr M: 0.01 – 0.01 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Location of the MT-CO2 gene in the human mitochondrial genome. MT-CO2 is one of the three cytochrome c oxidase subunit mitochondrial genes (orange boxes ...
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).
4 Fe 2+ – cytochrome c + 4 H + + O 2 → 4 Fe 3+ – cytochrome c + 2 H 2 O ΔG o ' = - 218 kJ/mol, E o ' = +565 mV. Two electrons are passed from two cytochrome c's, through the Cu A and cytochrome a sites to the cytochrome a 3 –Cu B binuclear center, reducing the metals to the Fe 2+ form and Cu +.
Once the COX-2 enzyme was identified, Dup-697 became the building-block for synthesis of COX-2 inhibitors. Celecoxib and rofecoxib, the first COX-2 inhibitors to reach market, were based on DuP-697. [ 5 ] [ 6 ] It took less than eight years to develop and market the first COX-2 inhibitor, with Celebrex ( celecoxib ) launched in December 1998 ...