Fig. 2

Ca²⁺/calmodulin inhibitor and endocytic inhibitors rescue filopodia during ER depletion. Cells were exposed to 5 µM CPA in Ca²⁺-free HBSS to deplete the ER of Ca²⁺. Inhibitors were used at final concentrations of 1–3 times the IC50 for the targeted activity. Means of 3–7 experiments are shown ± S.E.M. a, b Filopodia prevalence in the presence or absence of an inhibitor of calpain (ALLN), CaMKII (10 µM autocamtide-2 related inhibitory peptide), Ca²⁺/calmodulin (20 µM CALP2), or calcineurin (20 µM calcineurin-autoinhibitory peptide II). a Significance by ANOVA, P = 0.035. *Treatments differ at P = 0.037. b Significance by ANOVA, P = 0.0089. **P = 0.038. ***P = 0.0045. c, d Filopodia prevalence in the presence or absence of 0.4 M sucrose, 48 µM dynasore, 23 nM (-)-englerin, or 24 µM protein kinase C inhibitor (PKCI). c Significance by ANOVA, P = 0.0023. *Treatments differ at P = 0.0032. **P = 0.041. d Significance by ANOVA, P = 0.0032. (E, F) Filopodia prevalence in the presence or absence of W-7 (60 µM), 8-bromocyclic AMP (80 µM), K252a (50 nM), or wortmannin (1 µM). e Significance by ANOVA, P = 0.00001. ^†Treatments differ at P = 0.0032. ^††P = 0.0004. f Significance by ANOVA, P = 0.00001. ^†††Treatments differ at P = 0.0056. ^††††P = 0.0012. g, h Filopodia prevalence in the presence or absence of 20 µg/ml brefeldin A