Abstract
An antibody raised against a peptide in the first nucleotide-binding domain (NBD) of CFTR [1], incorporated into intact rat submandibular acini by hypotonic swelling, inhibited beta-adrenergic stimulated mucin secretion, without affecting cyclic AMP rise. The data are the first to show that a CFTR-antibody-containing cell results in defective stimulation of mucin secretion, as is seen in CF cells, and that this can be reversed by an excessive increase in cyclic AMP.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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1-Methyl-3-isobutylxanthine / pharmacology
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Adenosine Triphosphate / analysis
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Adrenergic beta-Agonists / pharmacology*
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Animals
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Antibodies / pharmacology*
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Cyclic AMP / analogs & derivatives
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Cyclic AMP / analysis
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Cyclic AMP / pharmacology
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Cystic Fibrosis / metabolism*
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Cystic Fibrosis Transmembrane Conductance Regulator
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Dose-Response Relationship, Drug
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Humans
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Isoproterenol / pharmacology
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Membrane Proteins / immunology*
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Mucins / metabolism*
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Peptide Fragments / immunology
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Rats
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Submandibular Gland / cytology
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Submandibular Gland / drug effects*
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Thionucleotides / pharmacology
Substances
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Adrenergic beta-Agonists
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Antibodies
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CFTR protein, human
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Membrane Proteins
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Mucins
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Peptide Fragments
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Thionucleotides
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Cystic Fibrosis Transmembrane Conductance Regulator
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8-((4-chlorophenyl)thio)cyclic-3',5'-AMP
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Adenosine Triphosphate
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Cyclic AMP
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Isoproterenol
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1-Methyl-3-isobutylxanthine