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• W4310219792 startingPage "775" @default.
• W4310219792 abstract "Background and Purpose Pharmacological inhibitors of TMEM16A (ANO1), a Ca2+-activated Cl− channel, are important tools of research and possible therapeutic agents acting on smooth muscle, airway epithelia and cancer cells. We tested a panel of TMEM16A inhibitors, including CaCCinh-A01, niclosamide, MONNA, Ani9 and niflumic acid, to evaluate their possible effect on intracellular Ca2+. Experimental Approach We recorded cytosolic Ca2+ increase elicited with UTP, ionomycin or IP3 uncaging. Key Results Unexpectedly, we found that all compounds, except for Ani9, markedly decreased intracellular Ca2+ elevation induced by stimuli acting on intracellular Ca2+ stores. These effects were similarly observed in cells with and without TMEM16A expression. We investigated in more detail the mechanism of action of niclosamide and CaCCinh-A01. Acute addition of niclosamide directly increased intracellular Ca2+, an activity consistent with inhibition of the SERCA pump. In contrast to niclosamide, CaCCinh-A01 did not elevate intracellular Ca2+, thus implying a different mechanism of action, possibly a block of inositol triphosphate receptors. Conclusions and Implications Most TMEM16A inhibitors are endowed with indirect effects mediated by alteration of intracellular Ca2+ handling, which may in part preclude their use as TMEM16A research tools." @default.
• W4310219792 created "2022-11-30" @default.
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• W4310219792 date "2022-12-18" @default.
• W4310219792 modified "2023-10-17" @default.
• W4310219792 title "Analysis of inhibitors of the anoctamin‐1 chloride channel (transmembrane member 16A, TMEM16A) reveals indirect mechanisms involving alterations in calcium signalling" @default.
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• W4310219792 doi "https://doi.org/10.1111/bph.15995" @default.
• W4310219792 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36444690" @default.
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