Effects of an inhibitor of tripeptidyl peptidase II (Ala-Ala-Phe-chloromethylketone) and its combination with an inhibitor of the chymotrypsin-like activity of the proteasome (PSI) on apoptosis, cell cycle and proteasome activity in U937 cells.

摘要: AAF-AMC is not a specific TPP II substrate, since it also hydrolyzed by purified proteasomes. Moreover, AAF-cmk, claimed to be inhibitor, inhibits the chymotrypsin-like activity of proteasome. While AAF-cmk itself mildly cytostatic U-937 cells and induces cell cycle block in G1, its combination with PSI does induce an increase cytostatic/cytotoxic effects. This suggests that possibly less important for metabolism than was previously believed probable can able fully compensate loss proteasome function.