Abstract
Heat-stable enterotoxin, produced by Escherichia coli, binds to particulate guanylate cyclase to increase cyclic GMP in intestinal cells. This in turn stimulates the cyclic-GMP- or cyclic-AMP-dependent protein kinase, activating the same chloride channel that is defective in cystic fibrosis. It is possible that the relatively high prevalence of cystic fibrosis in humans results from its protective effect against diarrhea.
Publication types
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Bacterial Toxins / pharmacology
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Chloride Channels / metabolism*
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Cyclic GMP / metabolism
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Cystic Fibrosis / genetics
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Cystic Fibrosis / metabolism*
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Cystic Fibrosis Transmembrane Conductance Regulator
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Diarrhea / metabolism*
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Enterotoxins / pharmacology
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Escherichia coli Infections / metabolism*
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Escherichia coli Proteins
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Humans
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Ion Transport / physiology
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Membrane Proteins / genetics
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Membrane Proteins / metabolism
Substances
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Bacterial Toxins
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CFTR protein, human
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Chloride Channels
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Enterotoxins
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Escherichia coli Proteins
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Membrane Proteins
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heat stable toxin (E coli)
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Cystic Fibrosis Transmembrane Conductance Regulator
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Cyclic GMP