Fig. 1: Bcl-xL overexpression inhibits IP3R-mediated Ca2+ release in living cells. | Cell Death & Differentiation

Fig. 1: Bcl-xL overexpression inhibits IP3R-mediated Ca2+ release in living cells.

From: Bcl-xL acts as an inhibitor of IP3R channels, thereby antagonizing Ca2+-driven apoptosis

Fig. 1

Ca2+ signals were measured in Fura-2-loaded HEK cells expressing empty vector (pCMV24-P2A-mCherry; black), Bcl-2 (pCMV24-3xFLAG-Bcl-2-P2A-mCherry; orange) or Bcl-xL (pCMV24-3xFLAG-Bcl-xL-P2A-mCherry; green). EGTA (3 mM) was added to chelate extracellular Ca2+. IP3R-mediated Ca2+ release was evoked by ATP (10 µM) (ae) or carbachol (Cch, 10 µM) (fj). Ionomycin (iono, 5 µM diluted in 250 mM CaCl2) was added to assess the maximal Ca2+ response. Representative single-cell Ca2+ responses obtained from one well containing about 20–40 cells are shown (ac, fh). For each condition, six to nine different wells obtained from two to three independent transfections were monitored. Percentages of responding cells (d, i) and areas under the curve (e, j) were calculated from the Ca2+ traces. Data are represented as mean of wells ± SD (N = 6–9), each data point represents one well. Statistically significant differences were determined using a one-way ANOVA (*P < 0.05).

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