NDLI: ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells.

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ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells.

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ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Liwei Ma, Wenbo Zhu, Linyan Ye, Dong Li, Yuan Liu, Shanwen Li, Huarong Zuo, Wanhong Li, Bingxue Ye, Wencai Chen, Lixin
Description	Country affiliation: China Author Affiliation: Wang L ( Department of Physiology, Medical College, Jinan University, Guangzhou, China. wangliweic@sohu.com)
Abstract	Acid-activated chloride currents have been reported in several cell types and may play important roles in regulation of cell function. However, the molecular identities of the channels that mediate the currents are not defined. In this study, activation of the acid-induced chloride current and the possible candidates of the acid-activated chloride channel were investigated in human nasopharyngeal carcinoma cells (CNE-2Z). A chloride current was activated when extracellular pH was reduced to 6.6 from 7.4. However, a further decrease of extracellular pH to 5.8 inhibited the current. The current was weakly outward-rectified and was suppressed by hypertonicity-induced cell shrinkage and by the chloride channel blockers 5-nitro-2-3-phenylpropylamino benzoic acid (NPPB), tamoxifen, and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt hydrate (DIDS). The permeability sequence of the channel to anions was I(-) > Br(-) > Cl(-) > gluconate(-). Among the ClC chloride channels, ClC-3 and ClC-7 were strongly expressed in CNE-2Z cells. Knockdown of ClC-3 expression with ClC-3 small interfering (si)RNA prevented the activation of the acid-induced current, but silence of ClC-7 expression with ClC-7 siRNA did not significantly affect the current. The results suggest that the chloride channel mediating the acid-induced chloride current was volume sensitive. ClC-3 is a candidate of the channel proteins that mediate or regulate the acid-activated chloride current in nasopharyngeal carcinoma cells.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
Journal	American Journal of Physiology - Cell Physiology
Issue Number	1
Volume Number	303
Language	English
Publisher	American Physiological Society
Publisher Date	2012-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Chloride Channels Metabolism Chlorides Nasopharyngeal Neoplasms 4,4'-diisothiocyanostilbene-2,2'-disulfonic Acid Pharmacology Cell Line, Tumor Antagonists & Inhibitors Genetics Membrane Potentials Drug Effects Nitrobenzoates Patch-clamp Techniques Rna Interference Rna, Small Interfering Tamoxifen Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells.

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ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells.