The Cdc42 inhibitor secramine B prevents cAMP-induced K+ conductance in intestinal epithelial cells

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The Cdc42 inhibitor secramine B prevents cAMP-induced K+ conductance in intestinal epithelial cells

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Title: The Cdc42 inhibitor secramine B prevents cAMP-induced K+ conductance in intestinal epithelial cells
Author: Pelish, Henry Efrem; Ciesla, William; Tanaka, Nori; Reddy, Krishna Podditur; Shair, Matthew David; Kirchhausen, Tomas Leopold; Lencer, Wayne Isaac

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Citation: Pelish, Henry E., William Ciesla, Nori Tanaka, Krishna Reddy, Matthew D. Shair, Tomas Kirchhausen, and Wayne I. Lencer. 2006. “The Cdc42 Inhibitor Secramine B Prevents cAMP-Induced K+ Conductance in Intestinal Epithelial Cells.” Biochemical Pharmacology 71 (12) (June): 1720–1726. doi:10.1016/j.bcp.2006.03.011.
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Abstract: Cyclic AMP- (cAMP) and calcium-dependent agonists stimulate chloride secretion through the coordinated activation of distinct apical and basolateral membrane channels and ion transporters in mucosal epithelial cells. Defects in the regulation of Cl– transport across mucosal surfaces occur with cystic fibrosis and V. cholerae infection and can be life threatening. Here we report that secramine B, a small molecule that inhibits activation of the Rho GTPase Cdc42, reduced cAMP-stimulated chloride secretion in the human intestinal cell line T84. Secramine B interfered with a cAMP-gated and Ba2+-sensitive K+ channel, presumably KCNQ1/KCNE3. This channel is required to maintain the membrane potential that sustains chloride secretion. In contrast, secramine B did not affect the Ca2+-mediated chloride secretion pathway, which requires a separate K+ channel activity from that of cAMP. Pirl1, another small molecule structurally unrelated to secramine B that also inhibits Cdc42 activation in vitro, similarly inhibited cAMP-dependent but not Ca2+-dependent chloride secretion. These results suggest that Rho GTPases may be involved in the regulation of the chloride secretory response and identify secramine B an inhibitor of cAMP-dependent K+ conductance in intestinal epithelial cells.
Published Version: doi:10.1016/j.bcp.2006.03.011
Other Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511784/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:33464219
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