Cdc42 prevents apoptosis by posttranscriptional stabilization of Bcl-2. (A) Immunoblot analysis of extracts prepared from 3 cA2K^b-Cdc42 and 3 cA2K^b-control fibrosarcomas. Note the increase in Bcl-2 levels in the Cdc42-expressing tumors. (B) Immunoblot analysis of cA2K^b-Cdc42 and cA2K^b-control MEFs following treatment with the translation inhibitor cycloheximide (CHX; 200 μg/mL) for up to 6 hours. Note the enhancement of Bcl-2 stability in cA2K^b-Cdc42 MEFs. (C) Etoposide treatment (12.5 μM) of cA2K^b-Cdc42 (■) and cA2K^b-control MEFs (□) incubated with ABT-737 (6.25 μM) or vehicle under low serum conditions. Apoptotic DNA fragmentation was quantified by flow cytometry following staining with propidium iodide; mean values plus SD of 3 experiments are shown.