Inhibit conversion of N-terminal Q to pE. formation of pE was prevented by inhibiting isoQC, CCL2 was more prone to N-terminal degradation, which resulted in less functional CCL2 activity. This had the net effect of decreasing monocyte infiltration in vivo, resulting in decreased lung inflammation,
Inhibit conversion of N-terminal Q to pE. formation of pE was prevented by inhibiting isoQC, CCL2 was more prone to N-terminal degradation, which resulted in less functional CCL2 activity. This had the net effect of decreasing monocyte infiltration in vivo, resulting in decreased lung inflammation.
