RecIAP plays a role in TNF-α secretion through ATP dephosphorylation
Since the use of recIAP in treating endotoxin-associated colitis (Lukas, 2010) has already been validated by clinical trials sponsored by AM-Pharma, this suggests that recIAP’s ability to dephosphorylate ATP is intimately related to the enzyme’s ability to suppress local ATP-induced inflammation generated by intestinal microorganisms (Lalles, 2014). The results of this study indicate that recIAP dephosphorylates ATP, ADP, and AMP in a dose-dependent manner and produces the products ADP, AMP, and adenosine, respectively (Figure 5 ABC). This study also finds that the ATP dephosphorylation products AMP and adenosine inhibit TNF-α secretion by human leukocytes (Figure 6 CD).