gpr39 is coupled to tmem16a in intestinal fibroblast-like cellsgpr39耦合在肠道tmem16a纤维母细胞.pdfVIP
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gpr39 is coupled to tmem16a in intestinal fibroblast-like cellsgpr39耦合在肠道tmem16a纤维母细胞
GPR39 Is Coupled to TMEM16A in Intestinal Fibroblast- Like Cells ¤ ¤ Fanning Zeng* , Nicholas Wind, Conor Mcclenaghan, J. Martin Verkuyl, Robert P. Watson, Mark S. Nash Gastrointestinal Disease Area, Novartis Horsham Research Centre, Horsham, United Kingdom Abstract GPR39 is a GPCR implicated as a regulator of gastrointestinal motility, although the mechanism remains elusive. Here, we report that GPR39 is expressed by a specific cell population cultured from mouse small intestine muscle layers, which was subsequently identified as fibroblast-like cells (FLCs) that have recently been shown to modulate gut motility. Application of the GPR39 agonist, Zn2+, induced large currents and membrane depolarization in FLCs cultured from wild-type mice, but not Gpr392/ 2 mice. This Zn2+-induced current could be suppressed by application of a TMEM16A antagonist, CaCCinh-A01, or by silencing Tmem16a expression. These data suggest that GPR39 might modulate gut motility via regulating TMEM16A function in FLCs. Citation: Zeng F, Wind N, Mcclenaghan C, Verkuyl JM, Watson RP, et al. (2012) GPR39 Is Coupled to TMEM16A in Intestinal Fibroblast-Like Cells. PLoS ONE 7(10): e47686. doi:10.1371/journal.pone.0047686 Editor: Adriano Marchese, Loyola University Chicago, Stritch School of Medicine, United States of America Received May 9, 2012; Accepted September 18, 2012; Published October 25, 2012 Copyright: 2012 Zeng et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: The authors have no support or funding to report. Competing Inter
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