Abstract
We examined the potential role of a guanine nucleotide-binding protein in the biosynthesis of paf-acether (paf) and the release of beta-hexosaminidase during antigenic stimulation of cultured mouse bone marrow-derived mast cells. Unlike pertussis toxin, cholera toxin treatment enhanced the antigen-stimulated production of paf and calcium mobilisation without affecting acetyltransferase activation and cell degranulation. The level of intracellular cAMP doubled in cholera toxin-treated cells. Our data suggest that a cholera toxin-sensitive guanine nucleotide-binding protein is involved in the IgE receptor-mediated signal transduction leading to paf production most probably at the level of Ca2+ influx.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetyltransferases / metabolism
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Animals
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Antigens, Differentiation, B-Lymphocyte / drug effects
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Antigens, Differentiation, B-Lymphocyte / physiology
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Bone Marrow / metabolism
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Bone Marrow Cells
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Calcium / metabolism*
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Cells, Cultured
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Cholera Toxin / pharmacology
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Cyclic AMP / metabolism
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GTP-Binding Proteins / metabolism*
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Immunoglobulin E / metabolism
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Kinetics
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Mast Cells / cytology
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Mast Cells / drug effects
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Mast Cells / metabolism*
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Mice
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Mice, Inbred BALB C
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Pertussis Toxin
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Platelet Activating Factor / biosynthesis*
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Receptors, Fc / drug effects
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Receptors, Fc / physiology
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Receptors, IgE
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Signal Transduction / drug effects
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Virulence Factors, Bordetella / pharmacology
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beta-N-Acetylhexosaminidases / metabolism
Substances
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Antigens, Differentiation, B-Lymphocyte
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Platelet Activating Factor
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Receptors, Fc
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Receptors, IgE
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Virulence Factors, Bordetella
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Immunoglobulin E
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Cholera Toxin
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Cyclic AMP
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Acetyltransferases
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Pertussis Toxin
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beta-N-Acetylhexosaminidases
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GTP-Binding Proteins
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Calcium