Figure 7.

(A) UCH-L1 siRNA treatment (50 nM) successfully silenced endogenous UCH-L1 expression in mock. MG132 (10 µM) treatment did not influence silencing of UCH-L1 in mock cells. (B) On UCH-L1 knockdown, Western blot analysis showed reduced ErbB1 and ErbB2 protein levels. However, in mock treated simultaneously with MG132 (10 µM) and siUCH-L1 (50 nM), this receptor down-regulation was abolished, suggesting that proteasome activity was essential for the degradation of ubiquitinated ErbB1/2. β-Actin was used to assess equal protein loading. (C) Silencing of UCH-L1 gene activity in mock resulted in an approximately 50% reduction in proliferation, which was similar to the growth rates determined for UCH-L1-negative EGFcyt transfectants.