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. Author manuscript; available in PMC: 2011 Dec 2.
Published in final edited form as: Cancer Res. 2009 Oct 6;69(20):7911–7916. doi: 10.1158/0008-5472.CAN-09-1287

Figure 1.

Figure 1

The PTEN-Akt pathway controls FLIPS protein stability. Mouse PTEN knockout or WT TMA or PTEN WT or mutant human xenografted GBM cells, or the same cells infected with a blank vector or construct encoding HA-ubiquitin (C), were incubated with vehicle or MG132 (10 µmol/L, 24 h; B), rapamycin (100 nmol/L, 24 h; D), or Akt III inhibitor (50 µmol/L, 24 h; D), after which cells were incubated with either vehicle or cycloheximide (CHX; 100 µg/mL; A, B, and D), lysed at the indicated time points, and analyzed either for levels of FLIPS and α-tubulin (A, B, D) or for the extent of HA ubiquitination in FLIPS immunoprecipitates (C). The α-tubulin blot shown in D is representative of those for all experimental groups.