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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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COX-3 the enzyme and the concept: steps towards highly specialized pathways and precision therapeutics?

Cyclooxygenases (COXs) catalyse the key rate-limiting step in prostanoid and thromboxane biosynthesis and are targets of non-steroidal anti-inflammatory drugs (NSAIDs). Until recently, the presence of only two isoforms-COX-1 and COX-2-remained in question because the potent anti-pyretic and analgesic effects of acetaminophen (paracetamol, tylenol ben-u-ron) could not be explained by either COX-1 or COX-2 blockades. A novel COX-1 splice variant termed COX-3, sensitive to acetaminophen, was recently discovered by Simmons et al., and is considered to play a key role in the biosynthesis of prostanoids known to be important mediators in pain and fever. Drugs that preferential block COX-1 also appear to act at COX-3. However the existence of COX-3 at the nucleotide sequence level in humans has been called to question. A functional COX-3 in humans is still to come underlining that the concept of COX-3 is still attractive. Here, we discuss some of the implications drawn from the identification of additional functional cyclooxygenase members in the generation of bioactive autacoids.[1]

References

  1. COX-3 the enzyme and the concept: steps towards highly specialized pathways and precision therapeutics? Schwab, J.M., Schluesener, H.J., Meyermann, R., Serhan, C.N. Prostaglandins Leukot. Essent. Fatty Acids (2003) [Pubmed]
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