Abstract
The ratio of late to early events stimulated by the mast cell receptor for immunoglobulin E (IgE) correlated with the affinity of a ligand for the receptor-bound IgE. Because excess receptors clustered by a weakly binding ligand could hoard a critical initiating kinase, they prevented the outnumbered clusters engendered by the high-affinity ligands from launching the more complete cascade. A similar mechanism could explain the antagonistic action of some peptides on the activation of T cells.
MeSH terms
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2,4-Dinitrophenol / immunology
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Adaptor Proteins, Signal Transducing
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Animals
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Antibody Affinity
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Antigen-Antibody Reactions
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism
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Dansyl Compounds
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Enzyme Precursors / metabolism
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Focal Adhesion Kinase 2
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Haptens / immunology*
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Haptens / metabolism
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Immunoglobulin E / immunology
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Immunoglobulin E / metabolism*
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Intracellular Signaling Peptides and Proteins
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Ligands
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Mast Cells / immunology*
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Mitogen-Activated Protein Kinase 1
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Oncogene Proteins / metabolism
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Phosphorylation
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Phosphotyrosine / metabolism
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Protein-Tyrosine Kinases / metabolism
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Rats
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Receptor Aggregation
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Receptors, IgE / immunology
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Receptors, IgE / metabolism*
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Signal Transduction
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Syk Kinase
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T-Lymphocytes / immunology
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Tumor Cells, Cultured
Substances
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Adaptor Proteins, Signal Transducing
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Dansyl Compounds
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Enzyme Precursors
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Haptens
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Intracellular Signaling Peptides and Proteins
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Ligands
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Nck protein
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Oncogene Proteins
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Receptors, IgE
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Phosphotyrosine
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Immunoglobulin E
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Protein-Tyrosine Kinases
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Focal Adhesion Kinase 2
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Ptk2b protein, rat
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Syk Kinase
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Syk protein, rat
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Calcium-Calmodulin-Dependent Protein Kinases
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Mitogen-Activated Protein Kinase 1
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2,4-Dinitrophenol