Fig. 4.

ERdj5 is a noncompetitive modulator of IP3Rs. (A) Effect of endogenous ERdj5 on IP3-IICR. After transfection with Yellow Cameleon 3.6 (YC 3.6) into WT or ERdj5-deficient HeLa cells, the cells were stimulated with BK, and the signal was normalized to the measured peak amplitude. Dose-response curves of the mean peak amplitudes are shown. (B and C) Effect of ERdj5 in IP3 receptor 1 (IP3R1)/WT- or IP3R1/AACC mutant-expressing cells on BK-induced Ca²⁺ release (Upper) or thapsigargin (Tg)-stimulated Ca²⁺ leakage (Lower). Each tracing represents the mean ± SEM of three independent experiments. ns, not significant; ***P < 0.001. (D and E) Redox state of PA-tagged IP3R1/TMD5-6C. After transfection with the indicated cDNA into HEK-293T cells, the cells were incubated in the presence or absence of 10 mM DTT or 1 mM dipyridyl disulfide (DPS) after fixing the redox reaction with trichloroacetic acid (TCA) and solubilized in the presence or absence of 10 mM maleimide-polyethylene glycol (2K-PEG mal). Proteins were separated by SDS-PAGE, and immunoblotting was performed to detect IP3R1/TMD5-6 with an anti-PA antibody. OE: overexpression of ERdj5. (F) ERdj5-mediated maintenance of Ca²⁺ homeostasis in the ER.