Abstract
The B cell-specific transmembrane protein RP-105 belongs to the family of Drosophila toll-like proteins which are likely to trigger innate immune responses in mice and man. Here we demonstrate that the Src-family protein tyrosine kinase Lyn, protein kinase C beta I/II (PKCbetaI/II), and Erk2-specific mitogen-activated protein (MAP) kinase kinase (MEK) are essential and probably functionally connected elements of the RP-105-mediated signaling cascade in B cells. We also find that negative regulation of RP-105-mediated activation of MAP kinases by membrane immunoglobulin may account for the phenomenon of antigen receptor-mediated arrest of RP-105-mediated B cell proliferation.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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B-Lymphocytes / physiology*
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Calcium / metabolism
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Cell Division / physiology
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Cells, Cultured
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Drosophila Proteins*
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Enzyme Activation / immunology
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Flow Cytometry
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Immunoglobulin M / immunology
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Membrane Glycoproteins / immunology
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Membrane Glycoproteins / physiology*
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Membrane Proteins / immunology
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Mice
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Mice, Knockout
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Mitogen-Activated Protein Kinase Kinases
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Phosphorylation
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Protein Kinase C / physiology
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Protein Kinases / physiology
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Receptors, Cell Surface / immunology
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Receptors, Cell Surface / physiology*
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Signal Transduction / physiology
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Spleen / immunology
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Toll-Like Receptors
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src-Family Kinases / physiology
Substances
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Drosophila Proteins
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Immunoglobulin M
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Membrane Glycoproteins
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Membrane Proteins
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Receptors, Cell Surface
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Toll-Like Receptors
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Protein Kinases
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src-Family Kinases
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Protein Kinase C
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Mitogen-Activated Protein Kinase Kinases
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Calcium