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. 2014 Oct 24;5(22):11526–11540. doi: 10.18632/oncotarget.2578

Figure 2. Lack of PKC⍺ drives to a faster degradation of Cyclin B1.

Figure 2

(a) Gene expression analyses of Cyclin B1 in conditions of silencing or overexpression of PKC⍺. Cells were synchronized at G2/M. Cyclin B1 expression is not affected by modulation of PKC⍺. (b) PKC⍺ was silenced and, 48 hours later, transfected cells were divided in two aliquots: one used as control (PKC⍺ KD) and one treated with MG-132 for 2 hours (PKC⍺ KD + MG-132 2h) The treatment blocked Cyclin B1 degradation and led to its accumulation in the cells. No changes in PKC⍺ levels were detected. These evidences suggested that down-modulation of Cyclin B1 due to lack of PKC⍺ was ceased inhibiting the proteasome machinery. (c) PKC⍺ was silenced and cells synchronized at G2/M. Silencing of PKC⍺ (PKC⍺ KD) leads to an accumulation of p21 compared to the control (Scrambled). This effect is opposite to Cyclin B1 decrease. p21 was used as a marker of degradation for Cyclin B1.