Figure 6

BCA3 modulates p53 transcriptional activity. Analysis of bax-promoter-Luciferase reporter activation in response to dose of HA-BCA3 (a), HA-BCA3 with c-myc-HIV-1 PR(D25N) (b) transiently transfected in HEK-293 cells. (c) Endogenous levels of p53 and Bax in the extract of the HEK-293 cells transfected with increasing amounts of HA-BCA3. (d) Subcellular fractionation and detection of endogenous p53 from HEK-293 cells expressing increasing amounts of BCA3. (e) Protein control of cytosolic (C), mitochondrial (M) and nuclear (N) fractions purity: fractions were purified as described in Material and Methods and analyzed using antibody against cytochrome c (mitochondrial marker) and lamin A (nuclear marker) antibodies. (f) Mean percentage of apoptotic, Anexin-V positive cells expressing HIV-1 PR, BCA3 or both. Each experiment was performed in triplicate; the mean values of three independent experiments (with standard deviation) are shown. The p value was insignificant (p < 0.4700295) between HIV-1 PR and BCA3, represented by columns 1 and 2, respectively. HIV-1 PR + BCA3 expression on apoptosis was statistically significant, characterized by p < 0.0047547 and p < 0.0015748 for the cells expressing HIV-1 PR and BCA3, respectively.