Abstract
Mice with a targeted gene disruption of p85alpha, a regulatory subunit of phosphoinositide 3-kinase, had impaired B cell development at the pro-B cell stage, reduced numbers of mature B cells and peritoneal CD5+ Ly-1 B cells, reduced B cell proliferative responses, and no T cell-independent antibody production. These phenotypes are nearly identical to those of Btk-/- or xid (X-linked immunodeficiency) mice. These results provide evidence that p85alpha is functionally linked to the Btk pathway in antigen receptor-mediated signal transduction and is pivotal in B cell development and functions.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Agammaglobulinaemia Tyrosine Kinase
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Animals
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Antibody Formation
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Antigens, Ly / analysis
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Antigens, T-Independent / immunology
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B-Lymphocyte Subsets / cytology
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B-Lymphocyte Subsets / immunology
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B-Lymphocytes / cytology
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B-Lymphocytes / immunology*
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Bone Marrow / immunology
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CD5 Antigens / analysis
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Cell Survival
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Gene Targeting
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Genetic Linkage
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Immunologic Deficiency Syndromes / enzymology*
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Immunologic Deficiency Syndromes / genetics
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Immunologic Deficiency Syndromes / immunology
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Lymphocyte Count
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Lymphoid Tissue / immunology
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Mice
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Mutation
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Phenotype
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Phosphatidylinositol 3-Kinases / genetics
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Phosphatidylinositol 3-Kinases / metabolism*
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Protein-Tyrosine Kinases / genetics
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Protein-Tyrosine Kinases / metabolism
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Signal Transduction
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T-Lymphocytes / immunology
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X Chromosome
Substances
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Antigens, Ly
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Antigens, T-Independent
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CD5 Antigens
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Phosphatidylinositol 3-Kinases
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Protein-Tyrosine Kinases
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Agammaglobulinaemia Tyrosine Kinase
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Btk protein, mouse