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. 2017 Dec 18;596(2):217–229. doi: 10.1113/JP275175

Figure 2. TMEM16A/ANO1 and TMEM16F/ANO6 are activated by PLA2 and by lipid peroxidizing ROS.

Figure 2

A, summary of current densities in HEK293 cells overexpressing TMEM16A/ANO1 and TMEM16F/ANO6. Effect of PLA2 blockers ACA (20 μm) and BEL (30 μm) on spontaneous Cl− currents active at 37°C. B, activation of TMEM16A/ANO1 and TMEM16F/ANO6 whole cell currents by the PLA2 activator melittin (200 nm). C, summary of current densities and inhibition by CaCCinhAO1 (AO1, 20 μm), ACA and BEL. D and E, activation of TMEM16A/ANO1 and TMEM16F/ANO6 by acute exposure to the PLA2 activator N‐ethylmaleimide (NEM; 50 μm), or by a pipette filling solution containing active PLA2 (0.5 U ml−1). F and G, activation of TMEM16A/ANO1 and TMEM16F/ANO6 by ROS‐inducers staurosporine (Stauro, 2 μm/6 h) and by tert‐butyl hydroperoxide (tBHP; 100 μm/2 h). values are mean ± SEM (number of experiments). #Significant difference when compared to mock (P < 0.05, unpaired t test). *Significant inhibition by AO1, ACA or BEL (P < 0.05, paired t test).