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. 2019 Aug 8;4(15):e128414. doi: 10.1172/jci.insight.128414

Figure 2. Inhibition of TMEM16A and TMEM16F by niclosamide.

Figure 2

(A) TMEM16A whole-cell currents in TMEM16A-overexpressing HEK293 cells. The purinergic agonist UTP (100 μM) was used to activate TMEM16A. UTP-induced currents were inhibited by niclosamide (1 μM). (B and C) Concentration-dependent inhibition of TMEM16A by niclosamide (n = 5–7 cells). (D) Current/voltage relationship showing inhibition of TMEM16F expressed in HEK293 cells by niclosamide (n = 5 cells each). (E) Inhibition of endogenous TMEM16A/F expressed in HT-29 cells examined by iodide quenching. Rate of YFP quenching (AU/s) when applying 20 mM iodide to the extracellular bath solution. HT-29 cells stably overexpressing YFP were stimulated with 1 μM ionomycin. Per well, 100,000 cells were seeded (n = 6–8 wells for each concentration). Inset: Western blot indicating expression of TMEM16F in HT-29 cells. Data are reported as mean ± SEM. *Significant activation (P < 0.05; paired t test); #significant inhibition (P < 0.05; unpaired t test).