Figure 4. NCLX does not control CRAC channels through buffering of cytosolic Ca²⁺ or mitochondrial energization.

• A, B
  Analysis of Ca²⁺ (A) and Na⁺ (B) CRAC currents measured at −100 mV in HEK293T cells transfected with either siControl or siNCLX using the indicated concentrations of BAPTA (20 mM versus 50 mM) in the pipette solution to activate CRAC and buffer cytosolic Ca²⁺.
• C–E
  Electrophysiological CRAC recordings were performed on cells where store depletion was induced by the use of a pipette solution containing low buffering capacity (0.1 mM EGTA) with IP₃ (30 μM) and a cocktail to energize the mitochondria whose composition is listed in the Results section. Representative time courses of whole‐cell current development at −100 mV (D, E) and measured in Ca²⁺‐containing and DVF solutions, respectively, by comparison with siControl. At the end of recordings, 5 μM Gd³⁺ was used to inhibit CRAC currents. Representative I–V relationships of Ca²⁺ (D) and Na⁺ (E) CRAC in cells transfected with siControl or siNCLX are taken from traces in (C) where indicated by color‐coded asterisks. Statistical analysis on Ca²⁺ and Na⁺ CRAC currents measured at −100 mV (D, E).

Data information: The results are presented as the means ± SEM. *P < 0.05; **P < 0.01 ***P < 1E‐03. P‐values indicate the results of a one‐way ANOVA test followed by Tukey post hoc analysis (A, B) or unpaired Student's t‐test (C–E).