Chloride Channel Clinched

Abstract only A transmembrane protein induced in cytokine-treated bronchial epithelial cells seems to be a long-sought primary carrier of a voltage- and calcium-dependent chloride current. The origin of calcium-dependent chloride currents, required for cell excitability and fluid secretion, has been...

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Bibliographic Details
Published in:Science signaling 2008-10, Vol.1 (43)
Main Author: Kelner, Katrina L.
Format: Article
Language:English
Online Access:Get full text
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Summary:Abstract only A transmembrane protein induced in cytokine-treated bronchial epithelial cells seems to be a long-sought primary carrier of a voltage- and calcium-dependent chloride current. The origin of calcium-dependent chloride currents, required for cell excitability and fluid secretion, has been confusing. Taking an unusual approach , Caputo et al . (see the Perspective by Hartzell) identified the transmembrane protein TMEM16A as a key component. This chloride current is up-regulated when bronchial epithelial cells are treated with interleukin-4 (IL-4). By inhibiting each messenger RNA up-regulated by IL-4 using specific small interfering RNAs in bronchial epithelial cells, the authors were able to identify the gene responsible for the chloride current. Because defects in chloride transport underlie the pathology of cystic fibrosis, this discovery may offer leads into new treatments. A. Caputo, E. Caci, L. Ferrera, N. Pedemonte, C. Barsanti, E. Sondo, U. Pfeffer, R. Ravazzolo, O. Zegarra-Moran, L. J. V. Galietta, TMEM16A, a membrane protein associated with calcium-dependent chloride channel activity. Science 322 , 590-594 (2008). [Abstract] [Full Text] H. C. Hartzell, CaCl-ing channels get the last laugh. Science 322 , 534-535 (2008). [Summary] [Full Text]
ISSN:1945-0877
1937-9145
DOI:10.1126/scisignal.143ec371