Fig. 5: Bcl-xL at the ER interacts with IP3R and decreases IP3R Ca2+ permeability.
From: The endoplasmic reticulum pool of Bcl-xL prevents cell death through IP3R-dependent calcium release
A Representative curves of ER calcium release in WT, ER-xL and Mt-xL MEFs transfected with CEPIA-1er after 25μM m-3M3FBS (PLC agonist) injection. B Quantification of the slope coefficient of ER calcium release after PLC activation in MEFs. A Kruskall Wallis ‘s test was performed with NWT = 46, NER-xL = 51, NMt-xL = 43 (mean ± SEM; **, p < 0.01; ***, p < 0.001). C Representative curves of cytosolic Ca2+ increase assessed with 5 μM Fluoforte after Ionomycin injection in WT, ER-xL and Mt-xL MEFs. D Quantification of Ionomycin response. The ratio of fluorescence, indicating Ca2+ peak amplitude relative to WT, is shown. A Kruskall Wallis’s test was performed with NWT = 26, NER-xL = 26, NMt-xL = 26 (mean ± SEM; *, p < 0.05; **, p < 0.01; ***, p < 0.001). E-F. Quantification of ER calcium release normalized to A23187 maximal ionophore-induced Ca2+ release response through 45Ca2+ flux analysis. Dose-response curves are shown in E. Quantification performed at 10μM IP3 is shown in F. A one way ANOVA test was performed with NWT = 5, NER-xL = 5, NMt-xL = 5 (mean ± SEM; ns, non-statistically significant; *, p < 0.05; **, p < 0.01). IP3-induced Ca2+ release in Mt-Bcl-xL MEFs is increased, compared to wild-type MEFs and ER-Bcl-xL.
