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).