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Sci. Signal., 28 October 2008
Vol. 1, Issue 43, p. ec371
[DOI: 10.1126/scisignal.143ec371]


Neuroscience Chloride Channel Clinched

Katrina L. Kelner

Science, AAAS, Washington, DC 20005, USA

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]

Citation: K. L. Kelner, Chloride Channel Clinched. Sci. Signal. 1, ec371 (2008).

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