期刊
CURRENT OPINION IN PHARMACOLOGY
卷 3, 期 6, 页码 594-599出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2003.06.012
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资金
- NEI NIH HHS [EY13574] Funding Source: Medline
- NHLBI NIH HHS [HL73856, HL59198] Funding Source: Medline
- NIBIB NIH HHS [EB00415] Funding Source: Medline
- NIDDK NIH HHS [DK35124] Funding Source: Medline
- NATIONAL EYE INSTITUTE [R01EY013574] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL059198, R01HL073856] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF BIOMEDICAL IMAGING AND BIOENGINEERING [R37EB000415, R01EB000415] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R37DK035124, R01DK035124] Funding Source: NIH RePORTER
The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated Cl- channel expressed in epithelial cells in the airways, pancreas, intestine and other fluid-transporting tissues. Cystic fibrosis is caused by mutations in the CFTR, resulting in impaired Cl- transport and plasma membrane targeting. CFTR is expressed in the lumenal membrane of enterocytes, where it functions as the principal pathway for secretion of Cl- and fluid in enterotoxin-induced secretory diarrheas such as cholera. Small-molecule CFTR inhibitors reduce enterotoxin-induced intestinal fluid secretion in animal models. CFTR inhibition might also reduce intestinal fluid losses in cholera and possibly in other infectious and non-infectious diarrheas.
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