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Thiazolidinone CFTR inhibitor identified by high-throughput screening blocks cholera toxin–induced intestinal fluid secretion
Tonghui Ma, … , Luis J.V. Galietta, A.S. Verkman
Tonghui Ma, … , Luis J.V. Galietta, A.S. Verkman
Published December 1, 2002
Citation Information: J Clin Invest. 2002;110(11):1651-1658. https://doi.org/10.1172/JCI16112.
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Article

Thiazolidinone CFTR inhibitor identified by high-throughput screening blocks cholera toxin–induced intestinal fluid secretion

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Abstract

Research Article

Authors

Tonghui Ma, Jay R. Thiagarajah, Hong Yang, Nitin D. Sonawane, Chiara Folli, Luis J.V. Galietta, A.S. Verkman

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Figure 4

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Specificity of CFTR inhibition by CFTRinh-172. (a) Alternative Cl– chann...
Specificity of CFTR inhibition by CFTRinh-172. (a) Alternative Cl– channels. Left: UTP (100 μM) stimulated Ca2+-dependent Cl– secretion measured in short-circuit current measurements on airway epithelial cells in the absence and presence of 5 μM CFTRinh-172. Right: Volume-activated Cl– current (hypotonic 250 mosM/kg H2O) measured in whole-cell patch-clamp experiments on FRT cells. Currents were recorded in the absence and presence of 5 μM CFTRinh-172. (b) MDR-1 activity. 3H-vincristine accumulation in 9HTEo-/Dx cells with upregulated MDR-1 expression. Intracellular vincristine was measured with and without verapamil (100 μM) or CFTRinh-172 (5 μM) (SE; n = 3). (c) ATP-sensitive K+ channels. Left: Representative membrane potential recording from a pancreatic β cell (INS-1) perfused extracellularly with CFTRinh-172, diazoxide (100 μM), and glibenclamide (glib; 10 μM). Right: Averaged changes in membrane potential (ΔmV) caused by indicated maneuvers (SE; n = 4). PD, potential difference.

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