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Cited by 1,088

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

CFTR as a cAMP-Dependent Regulator of Sodium Channels

Stutts, M. Jackson, Canessa, Cecilia M., Olsen, John C., Hamrick, Maura, Cohn, Jonathan A., Rossier, Bernard C., Boucher, Richard C.·1995·Science

Abstract

Cystic fibrosis transmembrane regulator (CFTR), the gene product that is mutated in cystic fibrosis (CF) patients, has a well-recognized function as a cyclic adenosine 3′,5′-monophosphate (cAMP)-regulated chloride channel, but this property does not account for the abnormally high basal rate and cAMP sensitivity of sodium ion absorption in CF airway epithelia. Expression of complementary DNAs for rat epithelial Na + channel (rENaC) alone in Madin Darby canine kidney (MDCK) epithelial cells generated large amiloride-sensitive sodium currents that were stimulated by cAMP, whereas coexpression of human CFTR with rENaC generated smaller basal sodium currents that were inhibited by cAMP. Parallel studies that measured regulation of sodium permeability in fibroblasts showed similar results. In CF airway epithelia, the absence of this second function of CFTR as a cAMP-dependent regulator likely accounts for abnormal sodium transport.

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Metadata

Authors
Stutts, M. J., Canessa, C. M., Olsen, J. C., Hamrick, M., Cohn, J. A., Rossier, B. C., & Boucher, R. C.
Venue
Science
Published
1995-08-11
Volume
269
Issue
5225
Pages
847-850
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2019099644
Cited by
1,088
References
1
FWCI
69.64
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: CFTR as a cAMP-Dependent Regulator of Sodium Channels. https://app.cochat.ai/papers/10.1126/science.7543698
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Stutts, M. J., Canessa, C. M., Olsen, J. C., Hamrick, M., Cohn, J. A., Rossier, B. C., & Boucher, R. C. (1995). CFTR as a cAMP-Dependent Regulator of Sodium Channels. Science. https://doi.org/10.1126/science.7543698

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