Fig. 2: BAPTAi caused MCL-1 downregulation and cell death in a Ca2+-independent manner.
Representative western blot and statistical analysis of BCL-2 (A, N = 9), BCL-XL (B, N = 6), BIM (C, N = 8), PUMA (D, N = 4) and MCL-1 (E, N = 10) levels normalized to untreated in response to vehicle (dark blue) and 10 µM of BAPTA-AM (red) after 2, 4, 6, and 8 h in OCI-LY-1 cells. Vinculin was included as a loading control. Data are represented as the average ± S.D. Statistically significant differences were determined with a paired two-tailed Student’s t test. Differences were considered significant when p < 0.05 (**p < 0.01; ***p < 0.001). F Representative western blot and densitometric analysis of MCL-1 levels in response to a 6 h treatment with of vehicle (dark blue), 10 µM EGTA-AM (light blue), TF-BAPTA-AM (yellow), DF-BAPTA-AM (orange), BAPTA-AM (red) and DM-BAPTA-AM (brown). Vinculin was included as a loading control. Data are represented as the average ± S.D. (N = 6). Statistically significant differences were determined with a paired ANOVA test. Differences were considered significant when p < 0.05 (**p < 0.01; ***p < 0.001). G Quantitative analysis of apoptosis in OCI-LY-1 in response to 6 h treatment with vehicle, 10 µM of EGTA-AM, TF-BAPTA-AM, DF-BAPTA-AM, BAPTA-AM and DM-BAPTA-AM. Cells were stained with annexin V-FITC and 7-AAD and the apoptotic fraction was identified as annexin V-positive cells. Data are represented as the average ± S.D. (N = 8). Statistically significant differences were determined with a paired ANOVA test. Differences were considered significant when p < 0.05 (**p < 0.01; ***p < 0.001).
